PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
28905270-3	2018	The findings were that diabetes induced by both doses of alloxan was accompanied by significant increases in the lysosomal activities of acid phosphatase and the glycosidases investigated: beta-glucuronidase, beta-galactosidase, beta-glucosidase, and N-acetyl-hexosaminidase.	Alloxan	57-64	glucuronidase, beta	Mus musculus	189-207
28816409-7	2018	In vivo, genistein also reduced fasting glucose levels accompanied with reduced PEPCK-C expression and increased in AMPK and ERK1/2 phosphorylation states in the liver of genistein-treated alloxan-induced diabetic mice.	Alloxan	189-196	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	116-120
28905270-3	2018	The findings were that diabetes induced by both doses of alloxan was accompanied by significant increases in the lysosomal activities of acid phosphatase and the glycosidases investigated: beta-glucuronidase, beta-galactosidase, beta-glucosidase, and N-acetyl-hexosaminidase.	Alloxan	57-64	galactosidase, beta 1	Mus musculus	209-227
28842434-5	2017	In response to an acute bolus intravenous injection of ANG II, alloxan-induced diabetic mice exhibited a higher mean arterial pressure (MAP) (119.1 +- 3.8 vs. 106.2 +- 3.5 mmHg) and a lower renal blood flow (0.25 +- 0.07 vs. 0.52 +- 0.14 ml/min) compared with nondiabetic mice.	Alloxan	63-70	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	55-61
28837876-7	2017	Importantly, phthalhydrazide treatment of alloxan-treated diabetic rats markedly decreased the concentrationof interleukin-6 (IL-6) and corticosterone level.	Alloxan	42-49	interleukin 6	Rattus norvegicus	111-124
28837876-7	2017	Importantly, phthalhydrazide treatment of alloxan-treated diabetic rats markedly decreased the concentrationof interleukin-6 (IL-6) and corticosterone level.	Alloxan	42-49	interleukin 6	Rattus norvegicus	126-130
28423281-9	2017	Alloxan induced degenerative changes in hepatic and pancreatic tissues, increased hepatic lipid peroxidation, and increased gene expression of PC and caspase 3.	Alloxan	0-7	caspase 3	Rattus norvegicus	150-159
28802580-7	2017	The repressive activity of BAP1 was relieved by alloxan but exacerbated by PUGNAc, an O-GlcNAcase (OGA) inhibitor.	Alloxan	48-55	Brca1 associated protein 1	Mus musculus	27-31
27114244-0	2016	Corrigendum to "BDNF protects pancreatic beta cells (RIN5F) against cytotoxic action of alloxan, streptozotocin, doxorubicin and benzo(a)pyrene in vitro" METABOLISM CLINICAL AND EXPERIMENTAL 65 (2016) 667-684.	Alloxan	88-95	brain derived neurotrophic factor	Homo sapiens	16-20
28190920-6	2017	Eight hours after AL treatment, aquaporin 1-negative and Na/K pump-positive thick ascending limbs of Henle (TAL) were degenerated in the outer medulla.	Alloxan	18-20	aquaporin 1	Rattus norvegicus	32-43
27776166-8	2016	In addition, GlcN-mediated O-GlcNAc modification was involved in the downregulation of TNF-alpha and IL-8 genes but not IL-6 and IL-24 genes, based on the effects of alloxan, an O-GlcNAc transferase inhibitor.	Alloxan	166-173	tumor necrosis factor	Homo sapiens	87-96
26908204-6	2016	Oral administration in the alloxan-induced diabetic mice of the mixture loaded in elastic anionic niosomes with the insulin doses at 25, 50 and 100 IU/kg body weight indicated significant hypoglycemic activity with the percentage fasting blood glucose reduction of 1.95, 2.10 and 2.10 folds of the subcutaneous insulin injection at 12 h, respectively.	Alloxan	27-34	insulin	Homo sapiens	116-123
26908204-6	2016	Oral administration in the alloxan-induced diabetic mice of the mixture loaded in elastic anionic niosomes with the insulin doses at 25, 50 and 100 IU/kg body weight indicated significant hypoglycemic activity with the percentage fasting blood glucose reduction of 1.95, 2.10 and 2.10 folds of the subcutaneous insulin injection at 12 h, respectively.	Alloxan	27-34	insulin	Homo sapiens	311-318
28220578-3	2017	Here, we hypothesize that "Alloxan-induced renal damage is associated with alterations of p53, TGF-beta1, and extracellular matrix metalloproteinases."	Alloxan	27-34	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	90-93
28220578-3	2017	Here, we hypothesize that "Alloxan-induced renal damage is associated with alterations of p53, TGF-beta1, and extracellular matrix metalloproteinases."	Alloxan	27-34	transforming growth factor, beta 1	Rattus norvegicus	95-104
27748816-3	2016	The current study investigated the effects of this compound (referred to as compound K16) on diabetes using an alloxan-induced diabetic mouse model.	Alloxan	111-118	keratin 16	Mus musculus	85-88
26452142-10	2015	An important fraction of the beta cells significantly lost insulin positivity after alloxan administration, which was restored to normal after one week of EGF/G treatment.	Alloxan	84-91	epidermal growth factor	Mus musculus	155-158
27085775-1	2016	OBJECTIVE: The study was conducted to observe whether brain-derived neurotrophic factor (BDNF) has cytoprotective actions against alloxan (AL), streptozotocin (STZ), doxorubicin (DB) and benzo(a)pyrene (BP) compounds in vitro that may account for its beneficial action in diabetes mellitus.	Alloxan	130-137	brain derived neurotrophic factor	Mus musculus	54-87
27085775-1	2016	OBJECTIVE: The study was conducted to observe whether brain-derived neurotrophic factor (BDNF) has cytoprotective actions against alloxan (AL), streptozotocin (STZ), doxorubicin (DB) and benzo(a)pyrene (BP) compounds in vitro that may account for its beneficial action in diabetes mellitus.	Alloxan	130-137	brain derived neurotrophic factor	Mus musculus	89-93
27085775-1	2016	OBJECTIVE: The study was conducted to observe whether brain-derived neurotrophic factor (BDNF) has cytoprotective actions against alloxan (AL), streptozotocin (STZ), doxorubicin (DB) and benzo(a)pyrene (BP) compounds in vitro that may account for its beneficial action in diabetes mellitus.	Alloxan	139-141	brain derived neurotrophic factor	Mus musculus	54-87
27085775-1	2016	OBJECTIVE: The study was conducted to observe whether brain-derived neurotrophic factor (BDNF) has cytoprotective actions against alloxan (AL), streptozotocin (STZ), doxorubicin (DB) and benzo(a)pyrene (BP) compounds in vitro that may account for its beneficial action in diabetes mellitus.	Alloxan	139-141	brain derived neurotrophic factor	Mus musculus	89-93
27085775-5	2016	Effect of alloxan, STZ, doxorubicin and BP on the production of BDNF by RIN5F cells was also studied.	Alloxan	10-17	brain derived neurotrophic factor	Mus musculus	64-68
27085775-6	2016	RESULTS: Results of the present study revealed that BDNF in the doses (100ng>50ng>10ng/ml) has significant cytoprotection (P<0.001, P<0.01) on cytotoxic action of AL, STZ, DB and BP against rat insulinoma RIN5F (5x10(4) cells/100mul) cells in vitro.	Alloxan	175-177	brain-derived neurotrophic factor	Rattus norvegicus	52-56
26827782-0	2016	Phycocyanin ameliorates alloxan-induced diabetes mellitus in mice: Involved in insulin signaling pathway and GK expression.	Alloxan	24-31	glucokinase	Mus musculus	109-111
26827782-6	2016	The results suggest that phycocyanin ameliorates alloxan-induced diabetes mellitus in mice by activating insulin signaling pathway and GK expression in pancreas and liver in diabetic mice.	Alloxan	49-56	glucokinase	Mus musculus	135-137
26664046-0	2015	Timosaponin B-II ameliorates diabetic nephropathy via TXNIP, mTOR, and NF-kappaB signaling pathways in alloxan-induced mice.	Alloxan	103-110	thioredoxin interacting protein	Mus musculus	54-59
26664046-0	2015	Timosaponin B-II ameliorates diabetic nephropathy via TXNIP, mTOR, and NF-kappaB signaling pathways in alloxan-induced mice.	Alloxan	103-110	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	71-80
25549789-1	2015	The effect of streptozotocin (STZ) and alloxan (ALX) on the hepatic messenger RNA (mRNA) expression of four transporters (Mrp2, Mdr1, Oct1, and Oatp1) was studied in the present work.	Alloxan	39-46	solute carrier organic anion transporter family, member 1a1	Rattus norvegicus	144-149
25549789-1	2015	The effect of streptozotocin (STZ) and alloxan (ALX) on the hepatic messenger RNA (mRNA) expression of four transporters (Mrp2, Mdr1, Oct1, and Oatp1) was studied in the present work.	Alloxan	48-51	ATP binding cassette subfamily C member 2	Rattus norvegicus	122-126
25549789-3	2015	The results indicated that the mRNA expression levels of the Mrp2, Mdr1, Oct1, and Oatp1 in ALX-induced diabetic rats, as well as the hepatic mRNA expression of Mdr1 and Oatp1 in STZ-induced diabetic rats, were significantly decreased as compared with the control.	Alloxan	92-95	ATP binding cassette subfamily C member 2	Rattus norvegicus	61-65
25549789-3	2015	The results indicated that the mRNA expression levels of the Mrp2, Mdr1, Oct1, and Oatp1 in ALX-induced diabetic rats, as well as the hepatic mRNA expression of Mdr1 and Oatp1 in STZ-induced diabetic rats, were significantly decreased as compared with the control.	Alloxan	92-95	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	67-71
25549789-3	2015	The results indicated that the mRNA expression levels of the Mrp2, Mdr1, Oct1, and Oatp1 in ALX-induced diabetic rats, as well as the hepatic mRNA expression of Mdr1 and Oatp1 in STZ-induced diabetic rats, were significantly decreased as compared with the control.	Alloxan	92-95	solute carrier family 22 member 1	Rattus norvegicus	73-77
25549789-3	2015	The results indicated that the mRNA expression levels of the Mrp2, Mdr1, Oct1, and Oatp1 in ALX-induced diabetic rats, as well as the hepatic mRNA expression of Mdr1 and Oatp1 in STZ-induced diabetic rats, were significantly decreased as compared with the control.	Alloxan	92-95	solute carrier organic anion transporter family, member 1a1	Rattus norvegicus	83-88
25105335-7	2015	On the other hand, we showed that alloxan administration was accompanied by an oxidative stress status assessed by an increase of malondialdehyde (MDA) and hydrogen peroxide (H2O2) levels, as well as a depletion of sulfhydril group content (-SH) and antioxidant enzyme activities as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in testis, epididymis, and sperm.	Alloxan	34-41	catalase	Rattus norvegicus	311-319
25105335-7	2015	On the other hand, we showed that alloxan administration was accompanied by an oxidative stress status assessed by an increase of malondialdehyde (MDA) and hydrogen peroxide (H2O2) levels, as well as a depletion of sulfhydril group content (-SH) and antioxidant enzyme activities as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in testis, epididymis, and sperm.	Alloxan	34-41	catalase	Rattus norvegicus	321-324
26855973-1	2015	The objective of this study is to detrmine whether alloxan-induced diabetic Lactoferrin knockout (LFKO-/-) mice are more susceptible to periodontal disease caused by Aggregatibacter actinomycetemcomitans compared to the diabetic wild-type (WT) mice.	Alloxan	51-58	lactotransferrin	Mus musculus	76-87
25199622-0	2015	Probucol prevents atrial remodeling by inhibiting oxidative stress and TNF-alpha/NF-kappaB/TGF-beta signal transduction pathway in alloxan-induced diabetic rabbits.	Alloxan	131-138	tumor necrosis factor	Oryctolagus cuniculus	71-80
25450901-0	2014	Expression of visfatin in alloxan-induced diabetic rat testis.	Alloxan	26-33	nicotinamide phosphoribosyltransferase	Rattus norvegicus	14-22
24939145-6	2014	Gene expression of TNF-alpha and TGF-beta1 showed gradual increase after one and two weeks of alloxan administration as compared to the normal group.	Alloxan	94-101	tumor necrosis factor	Rattus norvegicus	19-28
24939145-6	2014	Gene expression of TNF-alpha and TGF-beta1 showed gradual increase after one and two weeks of alloxan administration as compared to the normal group.	Alloxan	94-101	transforming growth factor, beta 1	Rattus norvegicus	33-42
24814361-2	2014	We sought to investigate the effects of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activator rosiglitazone on atrial structural remodeling and atrial fibrillation (AF) promotion in alloxan-induced diabetic rabbits.	Alloxan	200-207	peroxisome proliferator-activated receptor gamma	Oryctolagus cuniculus	90-100
25289966-5	2014	M. oleifera leaf extract counteracted the alloxan-induced diabetic effects in rats as it normalized the elevated serum levels of glucose, triglycerides, cholesterol, and malondialdehyde, and normalized mRNA expression of the gluconeogenic enzyme pyruvate carboxylase in hepatic tissues.	Alloxan	42-49	pyruvate carboxylase	Rattus norvegicus	246-266
24604151-4	2014	Supplementation of vanadium to alloxan-induced diabetic rats decreased the blood glucose levels due to hyperglycemia, inhibited the AR activity, and delayed cataract progression in a dose-dependent manner.	Alloxan	31-38	aldo-keto reductase family 1 member B1	Rattus norvegicus	132-134
24599112-4	2014	In this issue of Diabetologia (Brom et al DOI 10.1007/s00125-014-3166-3) it is reported that single photon emission computed tomography (SPECT) data with (111)indium-labelled glucagon-like peptide-1 (GLP-1) receptor agonist exendin-3 correlate with the morphometric analysis of beta cell mass in a rat model of alloxan-induced diabetes.	Alloxan	311-318	glucagon	Rattus norvegicus	175-198
24599112-4	2014	In this issue of Diabetologia (Brom et al DOI 10.1007/s00125-014-3166-3) it is reported that single photon emission computed tomography (SPECT) data with (111)indium-labelled glucagon-like peptide-1 (GLP-1) receptor agonist exendin-3 correlate with the morphometric analysis of beta cell mass in a rat model of alloxan-induced diabetes.	Alloxan	311-318	glucagon-like peptide 1 receptor	Rattus norvegicus	200-215
23880309-8	2013	HO-1 expression in islets was significantly upregulated in alloxan-injected Bach1-deficient mice, whereas expression of other antioxidative enzymes, e.g., catalase, superoxide dismutase, and glutathione peroxidase, was not changed by either alloxan administration or Bach1 deficiency.	Alloxan	59-66	heme oxygenase 1	Mus musculus	0-4
24711743-0	2014	The Control of Hyperglycemia by Estriol and Progesterone in Alloxan induced Type I Diabetes Mellitus Mice Model through Hepatic Insulin Synthesis.	Alloxan	60-67	insulin	Homo sapiens	128-135
24477542-8	2014	The oxytocin (OT) and vasopressin (VP) responses to insulin+glucose were blocked by the glucokinase inhibitor alloxan (4 mM; P <= 0.002) and the PI3K inhibitor wortmannin (50 nM; OT: P = 0.03; VP: P <= 0.002).	Alloxan	110-117	arginine vasopressin	Rattus norvegicus	22-33
24477542-8	2014	The oxytocin (OT) and vasopressin (VP) responses to insulin+glucose were blocked by the glucokinase inhibitor alloxan (4 mM; P <= 0.002) and the PI3K inhibitor wortmannin (50 nM; OT: P = 0.03; VP: P <= 0.002).	Alloxan	110-117	arginine vasopressin	Rattus norvegicus	35-37
24477542-8	2014	The oxytocin (OT) and vasopressin (VP) responses to insulin+glucose were blocked by the glucokinase inhibitor alloxan (4 mM; P <= 0.002) and the PI3K inhibitor wortmannin (50 nM; OT: P = 0.03; VP: P <= 0.002).	Alloxan	110-117	glucokinase	Rattus norvegicus	88-99
24477542-8	2014	The oxytocin (OT) and vasopressin (VP) responses to insulin+glucose were blocked by the glucokinase inhibitor alloxan (4 mM; P <= 0.002) and the PI3K inhibitor wortmannin (50 nM; OT: P = 0.03; VP: P <= 0.002).	Alloxan	110-117	arginine vasopressin	Rattus norvegicus	196-198
24331702-5	2014	To complement Rab18, and promote angiogenesis eNOS was also targeted, and this novel Rab18-eNOS therapy via a dynamically controlled "fibrin-in-fibrin" delivery system, demonstrated enhanced wound closure, by increasing functional angiogenesis and reducing inflammation, in an alloxan-induced hyperglycemic preclinical ear ulcer model of compromised wound healing.	Alloxan	277-284	RAB18, member RAS oncogene family	Homo sapiens	85-90
23880309-8	2013	HO-1 expression in islets was significantly upregulated in alloxan-injected Bach1-deficient mice, whereas expression of other antioxidative enzymes, e.g., catalase, superoxide dismutase, and glutathione peroxidase, was not changed by either alloxan administration or Bach1 deficiency.	Alloxan	59-66	BTB and CNC homology 1, basic leucine zipper transcription factor 1	Mus musculus	76-81
23539426-2	2013	This study investigated the hypoglycemic activity of orally delivered insulin - Tat mixture in alloxan-induced diabetic mice.	Alloxan	95-102	insulin	Homo sapiens	70-77
23970406-6	2013	In diabetic rats, gene expression of TNF-alpha and TGF-beta1 recorded a gradual increase and marked increase was observed after one and two weeks of alloxan administration, in comparison with normal rats.	Alloxan	149-156	tumor necrosis factor	Rattus norvegicus	37-46
23970406-6	2013	In diabetic rats, gene expression of TNF-alpha and TGF-beta1 recorded a gradual increase and marked increase was observed after one and two weeks of alloxan administration, in comparison with normal rats.	Alloxan	149-156	transforming growth factor, beta 1	Rattus norvegicus	51-60
22898325-3	2012	The working hypothesis was that alloxan-induced diabetes might modify the vascular effects of ANP in isolated rabbit renal arteries and the mechanisms involved in such actions.	Alloxan	32-39	natriuretic peptides A	Oryctolagus cuniculus	94-97
23138840-6	2013	ALX exposure elevated the blood glucose, serum ALP and ALT levels, the production of reactive oxygen species (ROS), and disturbed the intra-cellular antioxidant machineries.	Alloxan	0-3	PDZ and LIM domain 3	Rattus norvegicus	47-50
23092809-5	2013	Studies on the mechanism of apoptosis showed that ALX accelerated the markers of mitochondrial dependent apoptotic pathway (enhanced cytochrome C release in cytosol from mitochondria, altered the expression of Bax, Bcl-2, Apaf-1, caspase-9, caspase-3).	Alloxan	50-53	BCL2 associated X, apoptosis regulator	Rattus norvegicus	210-213
23092809-5	2013	Studies on the mechanism of apoptosis showed that ALX accelerated the markers of mitochondrial dependent apoptotic pathway (enhanced cytochrome C release in cytosol from mitochondria, altered the expression of Bax, Bcl-2, Apaf-1, caspase-9, caspase-3).	Alloxan	50-53	BCL2, apoptosis regulator	Rattus norvegicus	215-220
23092809-5	2013	Studies on the mechanism of apoptosis showed that ALX accelerated the markers of mitochondrial dependent apoptotic pathway (enhanced cytochrome C release in cytosol from mitochondria, altered the expression of Bax, Bcl-2, Apaf-1, caspase-9, caspase-3).	Alloxan	50-53	apoptotic peptidase activating factor 1	Rattus norvegicus	222-228
23092809-5	2013	Studies on the mechanism of apoptosis showed that ALX accelerated the markers of mitochondrial dependent apoptotic pathway (enhanced cytochrome C release in cytosol from mitochondria, altered the expression of Bax, Bcl-2, Apaf-1, caspase-9, caspase-3).	Alloxan	50-53	caspase 9	Rattus norvegicus	230-239
23092809-5	2013	Studies on the mechanism of apoptosis showed that ALX accelerated the markers of mitochondrial dependent apoptotic pathway (enhanced cytochrome C release in cytosol from mitochondria, altered the expression of Bax, Bcl-2, Apaf-1, caspase-9, caspase-3).	Alloxan	50-53	caspase 3	Rattus norvegicus	241-250
23667864-3	2013	The severity of hyperglycemia and hypertriglyceridemia decreased, hypercholesterolemia developed, hypotocoferolemia returned to normal, and the tendency to LPO inhibition was observed in rats 10 days after alloxan administration against the background of previous one-week treatment with insulin.	Alloxan	206-213	lactoperoxidase	Rattus norvegicus	156-159
23138840-10	2013	In addition, ALX exposure reciprocally regulated Bcl-2 family protein expression, disturbed mitochondrial membrane potential, and subsequently released cytochrome c from mitochondria to cytosol.	Alloxan	13-16	BCL2, apoptosis regulator	Rattus norvegicus	49-54
22356440-9	2012	The alloxan-induced decrease in the GK activity in islets and hepatocytes was also ameliorated by exendin-4 treatment.	Alloxan	4-11	glucokinase	Mus musculus	36-38
22728640-6	2012	IBP was administered orally at three doses [100, 200 and 400 mg/kg body weight] for 14 days to the diabetic mice induced by alloxan.	Alloxan	124-131	trafficking protein particle complex 9	Mus musculus	0-3
22659112-6	2012	Immunohistochemical studies in alloxan induced mice demonstrated a marked increase in the immunoreactivity of nuclear transcription factor (NF-kappaB).	Alloxan	31-38	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	140-149
22582095-10	2012	The study arrived at the conclusion that HC generates ROS in a redox-cycling reaction with Alx that explains the decline in viability of insulin-secreting cells, leading to reduced glucokinase phosphorylating ability, diminished insulin secretory responsiveness and cell death.	Alloxan	91-94	glucokinase	Rattus norvegicus	181-192
22239106-3	2012	Elevated levels of blood glucose, glycosylated Hb and TNFalpha decreased levels of plasma insulin and disturbed intra-cellular antioxidant machineries were detected in ALX exposed animals.	Alloxan	168-171	tumor necrosis factor	Rattus norvegicus	54-62
22239106-5	2012	Studies on the mechanism of ALX-induced diabetes showed that hyperglycemia caused disruption of mitochondrial membrane potential in the spleen, released cytochrome C in the cytosol, activated caspase 3 and ultimately led to apoptotic cell death.	Alloxan	28-31	caspase 3	Rattus norvegicus	192-201
22138235-10	2012	Results also suggest that taurine could protect cardiac tissue from ALX induced apoptosis via the regulation of Bcl2 family and caspase 9/3 proteins.	Alloxan	68-71	BCL2, apoptosis regulator	Rattus norvegicus	112-116
21981382-3	2012	Here, we used neuronal and murine models that overexpress human tau to demonstrate that mild oxidative stress generated by alloxan suppresses several phenotypes of tauopathy.	Alloxan	123-130	microtubule associated protein tau	Homo sapiens	64-67
21981382-4	2012	Alloxan treatment reduced HSP90 levels and promoted proteasomal degradation of tau, c-Jun N-amino terminal kinase, and histone deacetylase (HDAC) 6.	Alloxan	0-7	heat shock protein 86, pseudogene 1	Mus musculus	26-31
21981382-4	2012	Alloxan treatment reduced HSP90 levels and promoted proteasomal degradation of tau, c-Jun N-amino terminal kinase, and histone deacetylase (HDAC) 6.	Alloxan	0-7	microtubule associated protein tau	Homo sapiens	79-82
21981382-4	2012	Alloxan treatment reduced HSP90 levels and promoted proteasomal degradation of tau, c-Jun N-amino terminal kinase, and histone deacetylase (HDAC) 6.	Alloxan	0-7	jun proto-oncogene	Mus musculus	84-89
21981382-4	2012	Alloxan treatment reduced HSP90 levels and promoted proteasomal degradation of tau, c-Jun N-amino terminal kinase, and histone deacetylase (HDAC) 6.	Alloxan	0-7	histone deacetylase 6	Mus musculus	119-147
21981382-6	2012	Age-dependent decreases in HDAC2 and phospho-tau levels correlated with spatial memory enhancement in alloxan-injected tau mice.	Alloxan	102-109	histone deacetylase 2	Mus musculus	27-32
21981382-6	2012	Age-dependent decreases in HDAC2 and phospho-tau levels correlated with spatial memory enhancement in alloxan-injected tau mice.	Alloxan	102-109	microtubule associated protein tau	Homo sapiens	45-48
21981382-6	2012	Age-dependent decreases in HDAC2 and phospho-tau levels correlated with spatial memory enhancement in alloxan-injected tau mice.	Alloxan	102-109	microtubule associated protein tau	Homo sapiens	119-122
22138235-10	2012	Results also suggest that taurine could protect cardiac tissue from ALX induced apoptosis via the regulation of Bcl2 family and caspase 9/3 proteins.	Alloxan	68-71	caspase 9	Rattus norvegicus	128-137
21946410-0	2011	IGF1/insulin receptor kinase inhibition by BMS-536924 is better tolerated than alloxan-induced hypoinsulinemia and more effective than metformin in the treatment of experimental insulin-responsive breast cancer.	Alloxan	79-86	insulin like growth factor 1	Homo sapiens	0-4
22129064-4	2012	RHSE inhibited alloxan-induced nitric oxide (NO) generation through inhibition of inducible nitric oxide synthase (iNOS) gene expression and suppressed the inflammatory reaction in INS-1 cells through inhibition of expression of pro-inflammatory genes, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6).	Alloxan	15-22	nitric oxide synthase 2	Rattus norvegicus	82-113
22129064-4	2012	RHSE inhibited alloxan-induced nitric oxide (NO) generation through inhibition of inducible nitric oxide synthase (iNOS) gene expression and suppressed the inflammatory reaction in INS-1 cells through inhibition of expression of pro-inflammatory genes, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6).	Alloxan	15-22	nitric oxide synthase 2	Rattus norvegicus	115-119
22129064-4	2012	RHSE inhibited alloxan-induced nitric oxide (NO) generation through inhibition of inducible nitric oxide synthase (iNOS) gene expression and suppressed the inflammatory reaction in INS-1 cells through inhibition of expression of pro-inflammatory genes, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6).	Alloxan	15-22	tumor necrosis factor	Rattus norvegicus	263-290
22129064-4	2012	RHSE inhibited alloxan-induced nitric oxide (NO) generation through inhibition of inducible nitric oxide synthase (iNOS) gene expression and suppressed the inflammatory reaction in INS-1 cells through inhibition of expression of pro-inflammatory genes, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6).	Alloxan	15-22	tumor necrosis factor	Rattus norvegicus	292-301
22129064-4	2012	RHSE inhibited alloxan-induced nitric oxide (NO) generation through inhibition of inducible nitric oxide synthase (iNOS) gene expression and suppressed the inflammatory reaction in INS-1 cells through inhibition of expression of pro-inflammatory genes, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6).	Alloxan	15-22	interleukin 1 beta	Rattus norvegicus	304-321
22129064-4	2012	RHSE inhibited alloxan-induced nitric oxide (NO) generation through inhibition of inducible nitric oxide synthase (iNOS) gene expression and suppressed the inflammatory reaction in INS-1 cells through inhibition of expression of pro-inflammatory genes, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6).	Alloxan	15-22	interleukin 1 beta	Rattus norvegicus	323-331
22129064-4	2012	RHSE inhibited alloxan-induced nitric oxide (NO) generation through inhibition of inducible nitric oxide synthase (iNOS) gene expression and suppressed the inflammatory reaction in INS-1 cells through inhibition of expression of pro-inflammatory genes, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6).	Alloxan	15-22	interleukin 6	Rattus norvegicus	338-351
22129064-4	2012	RHSE inhibited alloxan-induced nitric oxide (NO) generation through inhibition of inducible nitric oxide synthase (iNOS) gene expression and suppressed the inflammatory reaction in INS-1 cells through inhibition of expression of pro-inflammatory genes, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6).	Alloxan	15-22	interleukin 6	Rattus norvegicus	353-357
22785400-5	2012	After 15 weeks, alloxan-treated diabetic rabbits with expected high blood glucose showed ~5-fold increase in Abeta40/Abeta42 in cortex and hippocampus, and significantly, generated Abeta-derived assemblies found in human AD.	Alloxan	16-23	amyloid beta precursor protein	Homo sapiens	109-114
21969757-4	2010	The erythrocytes membrane lipid peroxide and catalase activity was increased where as the activities of superoxide dismutase, glutathione peroxidase were found to be decreased significantly (P<0.01) in alloxan-induced diabetic rats.	Alloxan	205-212	catalase	Rattus norvegicus	45-53
20640461-5	2011	Here, we describe the synthesis of novel UDP-GlcNAc/UDP analogues and evaluate their inhibitory properties and structural binding modes in vitro alongside alloxan, a previously reported weak OGT inhibitor.	Alloxan	155-162	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	191-194
21705841-0	2011	Berberine ameliorates hyperglycemia in alloxan-induced diabetic C57BL/6 mice through activation of Akt signaling pathway.	Alloxan	39-46	thymoma viral proto-oncogene 1	Mus musculus	99-102
21998672-3	2011	In this paper, a number of alloxan-based compounds, initially conceived to bias other therapeutically relevant enzymes, were rationally modified and successfully repurposed to inhibit MMP-2 (also named gelatinase A) in the nanomolar range.	Alloxan	27-34	matrix metallopeptidase 2	Homo sapiens	184-189
21689743-5	2011	In addition, we found that Alloxan induces AMPK differently from IL1beta, as Alloxan acts mainly through CaMKII while IL1beta acts through LKB1 phosphorylation.	Alloxan	27-34	calcium/calmodulin-dependent protein kinase II, beta	Mus musculus	105-111
21689743-5	2011	In addition, we found that Alloxan induces AMPK differently from IL1beta, as Alloxan acts mainly through CaMKII while IL1beta acts through LKB1 phosphorylation.	Alloxan	27-34	interleukin 1 beta	Mus musculus	118-125
21689743-5	2011	In addition, we found that Alloxan induces AMPK differently from IL1beta, as Alloxan acts mainly through CaMKII while IL1beta acts through LKB1 phosphorylation.	Alloxan	27-34	serine/threonine kinase 11	Mus musculus	139-143
21689743-5	2011	In addition, we found that Alloxan induces AMPK differently from IL1beta, as Alloxan acts mainly through CaMKII while IL1beta acts through LKB1 phosphorylation.	Alloxan	77-84	calcium/calmodulin-dependent protein kinase II, beta	Mus musculus	105-111
21969757-5	2010	The levels of lipid peroxide in liver of diabetic rats increased significantly (P<0.01) and catalase, superoxide dismutase, glutathione peroxidase in liver was significantly decreased in alloxan-induced diabetic rats, when compared to normal rats.	Alloxan	190-197	catalase	Rattus norvegicus	95-103
20165912-2	2010	Alloxan, an inhibitor of O-GlcNAc transferase, potentiated responses of AMPA receptors composed of the GluR1 subunit expressed in Xenopus oocytes.	Alloxan	0-7	glutamate receptor, ionotropic, AMPA 1 L homeolog	Xenopus laevis	103-108
20600753-3	2010	Different works have demonstrated that NSF extract showed antihyperglycemic effect on alloxan-induced diabetic rats.	Alloxan	86-93	N-ethylmaleimide sensitive factor, vesicle fusing ATPase	Rattus norvegicus	39-42
20610567-7	2010	In an animal model of diabetes induced by alloxan, progression of hyperglycemia was significantly attenuated in mice given the Ad-GLP-1 vector compared with control mice.	Alloxan	42-49	glucagon	Mus musculus	130-135
20429050-9	2010	Our data also showed both that EMs inhibited cell apoptosis and cell cycle G1 arrest induced by STZ and ALX through down-regulaing p53 and p21 expression.	Alloxan	104-107	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	131-134
20429050-9	2010	Our data also showed both that EMs inhibited cell apoptosis and cell cycle G1 arrest induced by STZ and ALX through down-regulaing p53 and p21 expression.	Alloxan	104-107	KRAS proto-oncogene, GTPase	Rattus norvegicus	139-142
20447389-7	2010	Our results revealed that in alloxan-induced diabetic mice, the nuclear staining of NF-kappaB p65 was increased in glomerulus, whereas renal I kappaB-alpha protein was significantly reduced.	Alloxan	29-36	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	84-93
20447389-7	2010	Our results revealed that in alloxan-induced diabetic mice, the nuclear staining of NF-kappaB p65 was increased in glomerulus, whereas renal I kappaB-alpha protein was significantly reduced.	Alloxan	29-36	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	94-97
20447389-7	2010	Our results revealed that in alloxan-induced diabetic mice, the nuclear staining of NF-kappaB p65 was increased in glomerulus, whereas renal I kappaB-alpha protein was significantly reduced.	Alloxan	29-36	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	141-155
20130740-3	2010	HPS3 was selected for examination of its hypoglycemic mechanism because of its significant hypoglycemic effect in alloxan-induced diabetic mice.	Alloxan	114-121	HPS3, biogenesis of lysosomal organelles complex 2 subunit 1	Mus musculus	0-4
17768029-0	2009	Hepatic glucokinase activity is the primary defect in alloxan-induced diabetes of mice.	Alloxan	54-61	glucokinase	Mus musculus	8-19
20336201-6	2009	In vitro studies using cerebral extract from alloxan diabetic rats demonstrated significant (P<0.05) inhibition of AChE activity in the brain of normal animals.	Alloxan	45-52	acetylcholinesterase	Rattus norvegicus	118-122
20722995-1	2010	OBJECTIVES: In rats with diabetes mellitus induced by alloxan (DMIA) or streptozocin (DMIS), changes in the cytochrome P450 (CYP) isozymes in the liver, lung, kidney, intestine, brain, and testis have been reported based on Western blot analysis, Northern blot analysis, and various enzyme activities.	Alloxan	54-61	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	108-123
20722995-1	2010	OBJECTIVES: In rats with diabetes mellitus induced by alloxan (DMIA) or streptozocin (DMIS), changes in the cytochrome P450 (CYP) isozymes in the liver, lung, kidney, intestine, brain, and testis have been reported based on Western blot analysis, Northern blot analysis, and various enzyme activities.	Alloxan	54-61	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	125-128
19563792-8	2009	CONCLUSION: These results indicate that low catalase activity in the blood is associated with the diabetes mellitus caused by alloxan administration.	Alloxan	126-133	catalase	Mus musculus	44-52
19454312-1	2009	AIM OF THE STUDY: Total flavonids of Polygonatum(P) odoratum (TFP) were tested for anti-diabetic activity in streptozotocin (STZ)-induced diabetic mice and alloxan-induced diabetic rats.	Alloxan	156-163	tripartite motif-containing 39	Mus musculus	18-60
19454312-4	2009	The experiments were designed to detect the anti-diabetic activity of TFP by determination of blood glucose (BG) using one touch gluco-meter and insulin levels by using a radioimmunoassay kit in streptozotocin (STZ)-induced diabetic mice and alloxan-induced diabetic rats and alpha-amylase inhibitory activity by alpha-amylase inhibition assay in vitro.	Alloxan	242-249	tripartite motif-containing 39	Mus musculus	70-73
19454312-10	2009	TFP also could increase significantly the insulin level in alloxan-induced type 2 diabetic rats (P<0.05) compared with control.	Alloxan	59-66	tripartite motif-containing 39	Mus musculus	0-3
19268552-0	2009	The plasmid encoding HSP47 enhances collagen expression and promotes skin wound healing in an alloxan-induced diabetic model.	Alloxan	94-101	serine (or cysteine) peptidase inhibitor, clade H, member 1	Mus musculus	21-26
17768029-5	2009	Alloxan is believed to confer its diabetogenic effect by inhibiting pancreatic glucokinase activity, leading to pancreatic beta-cell death.	Alloxan	0-7	glucokinase	Mus musculus	79-90
17768029-7	2009	Our results show that alloxan treatment led to an 81% reduction in glucokinase immunoreactivity and a greater than 90% reduction in glucokinase enzymatic activity in the liver, suggesting that alloxan"s toxicity is not specific to the pancreas.	Alloxan	22-29	glucokinase	Mus musculus	67-78
17768029-7	2009	Our results show that alloxan treatment led to an 81% reduction in glucokinase immunoreactivity and a greater than 90% reduction in glucokinase enzymatic activity in the liver, suggesting that alloxan"s toxicity is not specific to the pancreas.	Alloxan	22-29	glucokinase	Mus musculus	132-143
18949387-8	2008	Of note, alloxan, an O-N-acetylglucosamine transferase inhibitor, which prevented the glucosamine-induced O-GlcNAc modification, abrogated the suppressive effect of glucosamine on MCP-1 and ICAM-1 expression (p<0.05 at 0.5 mM).	Alloxan	9-16	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	106-114
20830981-0	2009	Catalase activity, lipid peroxidation, cholesterol and triglyceride levels in alloxan--induced diabetes mellitus in female and male rats.	Alloxan	78-85	catalase	Rattus norvegicus	0-8
18711746-3	2009	The current study showed that alloxan-induced diabetic animals revealed hyperglycemia and was associated with an increase in the content of 5-HT, PKC-alpha expression and PKC activity (P < 0.05) simultaneously in striatum (ST), midbrain (MB), pons medulla (PM), cerebellum (CB), and cerebral cortex (CCX) from 7 days to 60 days.	Alloxan	30-37	protein kinase C, alpha	Rattus norvegicus	146-155
18711746-3	2009	The current study showed that alloxan-induced diabetic animals revealed hyperglycemia and was associated with an increase in the content of 5-HT, PKC-alpha expression and PKC activity (P < 0.05) simultaneously in striatum (ST), midbrain (MB), pons medulla (PM), cerebellum (CB), and cerebral cortex (CCX) from 7 days to 60 days.	Alloxan	30-37	protein kinase C, alpha	Rattus norvegicus	146-149
19120287-4	2008	The selection of ALR, for resistance against alloxan-induced free radical-mediated diabetes, led to a strain of mice with an elevated systemic as well as pancreatic ROS dissipation.	Alloxan	45-52	growth factor, augmenter of liver regeneration	Mus musculus	17-20
18949387-8	2008	Of note, alloxan, an O-N-acetylglucosamine transferase inhibitor, which prevented the glucosamine-induced O-GlcNAc modification, abrogated the suppressive effect of glucosamine on MCP-1 and ICAM-1 expression (p<0.05 at 0.5 mM).	Alloxan	9-16	C-C motif chemokine ligand 2	Homo sapiens	180-185
18949387-8	2008	Of note, alloxan, an O-N-acetylglucosamine transferase inhibitor, which prevented the glucosamine-induced O-GlcNAc modification, abrogated the suppressive effect of glucosamine on MCP-1 and ICAM-1 expression (p<0.05 at 0.5 mM).	Alloxan	9-16	intercellular adhesion molecule 1	Homo sapiens	190-196
19004374-2	2008	Pigs were made diabetic with single dose of alloxan, which acts by selectively destroying insulin-producing pancreatic beta cells thus inducing type 1 diabetes.	Alloxan	44-51	insulin	Sus scrofa	90-97
18478316-1	2008	PURPOSE: It has been reported that telithromycin is primarily metabolized via hepatic CYP3A1/2 in rats, the expression and/or mRNA level of hepatic CYP3A1/2 increase in rat model of diabetes mellitus induced by alloxan (DMIA) or streptozotocin (DMIS), and intestinal CYP3A1/2 enzyme activity decreases in rat model of DMIS.	Alloxan	211-218	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	148-154
18758143-8	2008	Furthermore, although oral administration of scutellarin (10 and 50 mg/kg) did not produce significant antihyperglycemic action, it lowered the serum MCP-1 levels significantly in alloxan-induced diabetic mice.	Alloxan	180-187	chemokine (C-C motif) ligand 2	Mus musculus	150-155
18690293-0	2008	PPAR gamma agonist normalizes glomerular filtration rate, tissue levels of homocysteine, and attenuates endothelial-myocyte uncoupling in alloxan induced diabetic mice.	Alloxan	138-145	peroxisome proliferator activated receptor gamma	Mus musculus	0-10
18478316-1	2008	PURPOSE: It has been reported that telithromycin is primarily metabolized via hepatic CYP3A1/2 in rats, the expression and/or mRNA level of hepatic CYP3A1/2 increase in rat model of diabetes mellitus induced by alloxan (DMIA) or streptozotocin (DMIS), and intestinal CYP3A1/2 enzyme activity decreases in rat model of DMIS.	Alloxan	211-218	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	148-154
18442208-0	2008	Ghrelin improves delayed gastrointestinal transit in alloxan-induced diabetic mice.	Alloxan	53-60	ghrelin	Mus musculus	0-7
19024533-9	2008	The relative values of nNOS mRNA expression 15, 30, and 45 days after alloxan injection of diabetic ED rabbits were 0.670 +/- 0.030, 0.451 +/- 0.012, and 0.206 +/- 0.023 respectively,all significantly lower than those of the control group (0.817 +/- 0.010, 0.814 +/- 0.020, and 0.802 +/- 0.007 respectively, all P < 0.05).	Alloxan	70-77	nitric oxide synthase, brain	Oryctolagus cuniculus	23-27
19024533-10	2008	Western blotting showed that the relative values of nNOS 15, 30, and 45 days after alloxan injection of the ED rabbits were 0.713 +/- 0.014, 0.424 +/- 0.007, and 0.337 +/- 0.009 respectively, all significantly lower than those of the control group (0.797 +/- 0.015, 0.706 +/- 0.020, and 0.	Alloxan	83-90	nitric oxide synthase, brain	Oryctolagus cuniculus	52-56
18516449-2	2008	METHODS: evaluations were performed in three groups: A--8 weeks of age, B--44 weeks of age, C--44 weeks of age with alloxan-induced diabetes.	Alloxan	116-123	alpha-1-B glycoprotein	Rattus norvegicus	92-97
18087688-1	2008	Alloxan and streptozotocin are toxic glucose analogues that preferentially accumulate in pancreatic beta cells via the GLUT2 glucose transporter.	Alloxan	0-7	solute carrier family 2 member 2	Homo sapiens	119-124
17116429-8	2007	Furthermore, UNG-proteins and SMUG1 may have important functions in removal of oxidized cytosines, e.g. isodialuric acid, alloxan and 5-hydroxyuracil after exposure to ionizing radiation.	Alloxan	122-129	uracil DNA glycosylase	Mus musculus	13-16
18212479-4	2008	Western blot and immunohistochemical analyses revealed that BPRP levels were decreased in the hippocampal CA1 neurons of diabetic rats 4 and 8 weeks post-alloxan injection and in PC12 cells 48 h after exposure to high concentrations of glucose.	Alloxan	154-161	carbonic anhydrase 1	Rattus norvegicus	106-109
18034661-8	2007	HSE at 200 mg/kg attenuated the alloxan-induced decrease in the activities of superoxide dismutase (SOD), catalase (CAT) and the level of glutathione (GSH) by 36%, 44%, and 64% in the liver and by 20%, 43%, and 85% in the kidney of rats.	Alloxan	32-39	catalase	Rattus norvegicus	106-114
18034661-8	2007	HSE at 200 mg/kg attenuated the alloxan-induced decrease in the activities of superoxide dismutase (SOD), catalase (CAT) and the level of glutathione (GSH) by 36%, 44%, and 64% in the liver and by 20%, 43%, and 85% in the kidney of rats.	Alloxan	32-39	catalase	Rattus norvegicus	116-119
17101234-4	2007	Although uracil is the main substrate of uracil-DNA glycosylases UNG1 and UNG2, these proteins also remove the oxidized cytosine derivatives isodialuric acid, alloxan and 5-hydroxyuracil.	Alloxan	159-166	uracil DNA glycosylase	Homo sapiens	65-69
17101234-4	2007	Although uracil is the main substrate of uracil-DNA glycosylases UNG1 and UNG2, these proteins also remove the oxidized cytosine derivatives isodialuric acid, alloxan and 5-hydroxyuracil.	Alloxan	159-166	uracil DNA glycosylase	Homo sapiens	74-78
17658282-6	2007	Under normal physiological conditions, or during diabetes induction with alloxan or multiple low doses of streptozotocin, blood glucose was significantly lower in mice overexpressing endothelial nitric oxide synthase compared to wildtype or knockout mice.	Alloxan	73-80	nitric oxide synthase 3, endothelial cell	Mus musculus	183-216
17116429-8	2007	Furthermore, UNG-proteins and SMUG1 may have important functions in removal of oxidized cytosines, e.g. isodialuric acid, alloxan and 5-hydroxyuracil after exposure to ionizing radiation.	Alloxan	122-129	single-strand-selective monofunctional uracil-DNA glycosylase 1	Homo sapiens	30-35
18806305-3	2007	While a single dose of alloxan (120 mg/kg) increased the serum levels of glucose and alpha-amylase activity, rate of water consumption and lipid peroxidation (LPO) in hepatic, cardiac and renal tissues with a parallel decrease in serum insulin level, administration of 25 mg/kg of CS or 200 mg/kg of PG was found to normalize all the adverse changes induced by alloxan, revealing the antidiabetic and anti peroxidative potential of test fruit peel extracts.	Alloxan	23-30	alpha-amylase	Citrus sinensis	85-98
17069847-8	2007	O-GlcNAc transferase (OGT) catalyzes the formation of O-GlcNAc, and inhibition of OGT with 5 mM alloxan also reversed the protection associated with glutamine.	Alloxan	96-103	O-linked N-acetylglucosamine (GlcNAc) transferase	Rattus norvegicus	0-20
17867477-0	2007	Effect of a compound recipe (medicinal plants) on serum insulin levels of alloxan induced diabetic rabbits.	Alloxan	74-81	insulin	Oryctolagus cuniculus	56-63
17867477-10	2007	CONCLUSION: From this study it may be concluded that the Compound recipe causes an increase in serum insulin levels in alloxan induced diabetic rabbits possibly due to regeneration of pancreatic beta cells.	Alloxan	119-126	insulin	Oryctolagus cuniculus	101-108
17069847-8	2007	O-GlcNAc transferase (OGT) catalyzes the formation of O-GlcNAc, and inhibition of OGT with 5 mM alloxan also reversed the protection associated with glutamine.	Alloxan	96-103	O-linked N-acetylglucosamine (GlcNAc) transferase	Rattus norvegicus	22-25
17069847-8	2007	O-GlcNAc transferase (OGT) catalyzes the formation of O-GlcNAc, and inhibition of OGT with 5 mM alloxan also reversed the protection associated with glutamine.	Alloxan	96-103	O-linked N-acetylglucosamine (GlcNAc) transferase	Rattus norvegicus	82-85
17045574-0	2006	Alloxan is an inhibitor of O-GlcNAc-selective N-acetyl-beta-D-glucosaminidase.	Alloxan	0-7	O-GlcNAcase	Homo sapiens	27-77
17146556-6	2006	Further characterization of this molecule by reverse-phase hydrophobic HPLC chromatographic analysis as well as its antidiabetic activity on alloxan-induced mice showed that it has insulin-like properties.	Alloxan	141-148	insulin	Sus scrofa	181-188
17045574-9	2006	Together, these data demonstrate that alloxan is an inhibitor of O-GlcNAc-selective N-acetyl-beta-d-glucosaminidase, with inhibition corresponding to an altered tryptic digest pattern of N-terminal active site peptides.	Alloxan	38-45	O-GlcNAcase	Homo sapiens	65-115
16753349-5	2006	For intravenous insulin/glucose infusion test, high-fat diet-fed and low-dose alloxan-treated Wistar rats were associated with insulin resistance, which was improved after AC or fenofibrate treatment.	Alloxan	78-85	insulin	Homo sapiens	16-23
16895803-1	2006	The diabetogenic agent alloxan is selectively accumulated in insulin-producing cells through uptake via the GLUT2 glucose transporter in the plasma membrane.	Alloxan	23-30	insulin	Homo sapiens	61-68
16895803-1	2006	The diabetogenic agent alloxan is selectively accumulated in insulin-producing cells through uptake via the GLUT2 glucose transporter in the plasma membrane.	Alloxan	23-30	solute carrier family 2 member 2	Homo sapiens	108-113
16753349-5	2006	For intravenous insulin/glucose infusion test, high-fat diet-fed and low-dose alloxan-treated Wistar rats were associated with insulin resistance, which was improved after AC or fenofibrate treatment.	Alloxan	78-85	insulin	Homo sapiens	127-134
16716913-12	2006	daily for 7 days, CSP-1 produced a significant drop in blood glucose level in both STZ-induced diabetic rats and alloxan-induced diabetic mice.	Alloxan	113-120	common salivary protein 1	Rattus norvegicus	18-23
16835866-4	2006	In addition, alloxan induced a notable increase in the expression of CD8+ lymphocytes to form a dramatic decrease in CD4+/CD8+ ratio (while CD4+ was unchanged).	Alloxan	13-20	CD4 antigen	Mus musculus	117-120
16567528-9	2006	The alloxan-induced approximately 60% deficit in beta-cell mass lead to an approximately 70% deficit in postprandial insulin secretion and loss of the postprandial insulin-driven suppression of glucagon secretion.	Alloxan	4-11	insulin	Sus scrofa	117-124
16516154-3	2006	In the present study, we therefore investigated apoM expression and secretion in NMRI mice rendered diabetes through administration of alloxan (120 mg/kg).	Alloxan	135-142	apolipoprotein M	Mus musculus	48-52
14985051-1	2004	The influence of alloxan-induced diabetes on the reactivity of rabbit basilar artery to endothelin-1 was examined.	Alloxan	17-24	endothelin-1	Oryctolagus cuniculus	88-100
16684669-0	2006	Interleukin-6 and oxidative stress in plasma of alloxan-induced diabetic rabbits after pioglitazone treatment.	Alloxan	48-55	interleukin-6	Oryctolagus cuniculus	0-13
15277373-6	2004	The glucokinase inhibitor alloxan increases KATP single-channel currents in glucose-excited neurons in a manner similar to low glucose.	Alloxan	26-33	glucokinase	Rattus norvegicus	4-15
15226592-4	2004	Our approach was to determine the effect of injecting alloxan, a GK inhibitor, into the 4V on pulsatile luteinizing hormone (LH) secretion.	Alloxan	54-61	glucokinase	Rattus norvegicus	65-67
15652272-3	2005	flowers (ACF) was screened for its antioxidant effect in alloxan induced diabetic rats.	Alloxan	57-64	APOBEC1 complementation factor	Rattus norvegicus	9-12
14758569-2	2004	Here, we describe differential in vitro effects of STZ and ALX on beta-cell molecules that are essential for glucose transport and metabolism, the glucose transporter 2 (GLUT2) and glucokinase (GK), respectively.	Alloxan	59-62	solute carrier family 2 (facilitated glucose transporter), member 2	Mus musculus	147-168
14666367-0	2004	Combined gastrin and epidermal growth factor treatment induces islet regeneration and restores normoglycaemia in C57Bl6/J mice treated with alloxan.	Alloxan	140-147	gastrin	Mus musculus	9-16
14666367-0	2004	Combined gastrin and epidermal growth factor treatment induces islet regeneration and restores normoglycaemia in C57Bl6/J mice treated with alloxan.	Alloxan	140-147	epidermal growth factor	Mus musculus	21-44
14758569-2	2004	Here, we describe differential in vitro effects of STZ and ALX on beta-cell molecules that are essential for glucose transport and metabolism, the glucose transporter 2 (GLUT2) and glucokinase (GK), respectively.	Alloxan	59-62	solute carrier family 2 (facilitated glucose transporter), member 2	Mus musculus	170-175
14758569-2	2004	Here, we describe differential in vitro effects of STZ and ALX on beta-cell molecules that are essential for glucose transport and metabolism, the glucose transporter 2 (GLUT2) and glucokinase (GK), respectively.	Alloxan	59-62	glucokinase	Mus musculus	181-192
14758569-2	2004	Here, we describe differential in vitro effects of STZ and ALX on beta-cell molecules that are essential for glucose transport and metabolism, the glucose transporter 2 (GLUT2) and glucokinase (GK), respectively.	Alloxan	59-62	glucokinase	Mus musculus	194-196
14758569-4	2004	ALX concentration-dependently reduced the mRNA expression of GLUT2 and GK and the effect on GLUT2 was more marked.	Alloxan	0-3	solute carrier family 2 (facilitated glucose transporter), member 2	Mus musculus	61-66
14758569-4	2004	ALX concentration-dependently reduced the mRNA expression of GLUT2 and GK and the effect on GLUT2 was more marked.	Alloxan	0-3	glucokinase	Mus musculus	71-73
14758569-4	2004	ALX concentration-dependently reduced the mRNA expression of GLUT2 and GK and the effect on GLUT2 was more marked.	Alloxan	0-3	solute carrier family 2 (facilitated glucose transporter), member 2	Mus musculus	92-97
14758569-11	2004	Preincubation with D-G, however, protected the cultures from ALX-induced reduction of GLUT2 and GK mRNA expression, whereas 5-T-G, at best, exerted a modest protection against ALX at a concentration of 1 mmol/l.	Alloxan	61-64	solute carrier family 2 (facilitated glucose transporter), member 2	Mus musculus	86-91
14758569-11	2004	Preincubation with D-G, however, protected the cultures from ALX-induced reduction of GLUT2 and GK mRNA expression, whereas 5-T-G, at best, exerted a modest protection against ALX at a concentration of 1 mmol/l.	Alloxan	61-64	glucokinase	Mus musculus	96-98
14614541-7	2003	Injection in alloxan-treated rats with purified recombinant fusion adiponectin or gAdiponectin transiently abolished hyperglycemia.	Alloxan	13-20	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	67-78
12625506-6	2003	Acute toxic effects of alloxan (hypoglycemia, hyperglycemia, nephrotoxicosis) were minimized by preventive fluid loading and by use of algorithms in which insulin, food, and fluid therapy were administered.	Alloxan	23-30	insulin	Sus scrofa	155-162
12928773-6	2003	RESULTS: MMP-9 activity, measured by zymography, increased in plasma and in the left ventricle of alloxan-induced diabetic wild-type mice.	Alloxan	98-105	matrix metallopeptidase 9	Mus musculus	9-14
14552552-3	2003	Preceding anxiogenic stress increased the extent of the alloxan-induced increase in cerebral MAO-B activity and the accompanying abnormalities in the rats" behavior, and also potentiated the hyperglycemic effect of alloxan.	Alloxan	56-63	monoamine oxidase B	Rattus norvegicus	93-98
12605241-1	2003	Corpus cavernosum smooth muscle (CCSM) from rabbits made diabetic for 6 months as a result of alloxan injection exhibited increased sensitivity (3vs 9 nM EC(50)) and generated 20-50% greater force to endothelin-1 (ET-1) compared to CCSM from normal rabbits.	Alloxan	94-101	endothelin-1	Oryctolagus cuniculus	200-212
12605241-1	2003	Corpus cavernosum smooth muscle (CCSM) from rabbits made diabetic for 6 months as a result of alloxan injection exhibited increased sensitivity (3vs 9 nM EC(50)) and generated 20-50% greater force to endothelin-1 (ET-1) compared to CCSM from normal rabbits.	Alloxan	94-101	endothelin-1	Oryctolagus cuniculus	214-218
12625507-11	2003	We conclude that hyperglycemia is a major cause of insulin resistance in the porcine model of alloxan-induced diabetes mellitus and dyslipidemia.	Alloxan	94-101	insulin	Sus scrofa	51-58
14598126-6	2003	With the use of the subcutaneous insulin lispro infusion algorithm, which we have previously reported, alloxan-induced diabetic dogs exhibited postprandial hyperglycemia and delayed hyperinsulinemia, followed by hypoglycemia after an oral glucose load of 2 g/kg.	Alloxan	103-110	insulin	Canis lupus familiaris	33-40
12054585-4	2002	In isolated pancreatic islets, alloxan almost completely blocked both glucosamine-induced and STZ-induced protein O-GlcNAcylation, suggesting that alloxan indeed was inhibiting (OGT).	Alloxan	31-38	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	178-181
12413707-4	2002	The extracts reduced blood glucose level 2 h following administration in both normal and alloxan-induced diabetic mice.	Alloxan	89-96	blood glucose level 2	Mus musculus	21-42
12137914-6	2002	Ex vivo, a gradual decrement of both GLUT2 and GK mRNA expression was found in islets isolated from ALX-treated C57BL/6 mice.	Alloxan	100-103	solute carrier family 2 (facilitated glucose transporter), member 2	Mus musculus	37-42
12137914-6	2002	Ex vivo, a gradual decrement of both GLUT2 and GK mRNA expression was found in islets isolated from ALX-treated C57BL/6 mice.	Alloxan	100-103	glucokinase	Mus musculus	47-49
12137914-9	2002	Pretreatment with D-glucose (D-G) protected the mRNA expression of GLUT2 and GK against ALX toxicity and prevented diabetes.	Alloxan	88-91	solute carrier family 2 (facilitated glucose transporter), member 2	Mus musculus	67-72
12137914-9	2002	Pretreatment with D-glucose (D-G) protected the mRNA expression of GLUT2 and GK against ALX toxicity and prevented diabetes.	Alloxan	88-91	glucokinase	Mus musculus	77-79
12436338-1	2002	AIMS/HYPOTHESIS: We investigated the importance of the low affinity GLUT2 glucose transporter in the diabetogenic action of alloxan in bioengineered RINm5F insulin-producing cells with different expressions of the transporter.	Alloxan	124-131	solute carrier family 2 member 2	Rattus norvegicus	68-73
12054585-4	2002	In isolated pancreatic islets, alloxan almost completely blocked both glucosamine-induced and STZ-induced protein O-GlcNAcylation, suggesting that alloxan indeed was inhibiting (OGT).	Alloxan	147-154	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	178-181
12054585-5	2002	In order to show definitively that alloxan was inhibiting OGT activity, recombinant OGT was incubated with 0-10 mM alloxan, and OGT activity was measured directly by quantitating UDP-[(3)H]-GlcNAc incorporation into the recombinant protein substrate, nucleoporin p62.	Alloxan	35-42	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	58-61
12054585-5	2002	In order to show definitively that alloxan was inhibiting OGT activity, recombinant OGT was incubated with 0-10 mM alloxan, and OGT activity was measured directly by quantitating UDP-[(3)H]-GlcNAc incorporation into the recombinant protein substrate, nucleoporin p62.	Alloxan	35-42	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	84-87
12054585-5	2002	In order to show definitively that alloxan was inhibiting OGT activity, recombinant OGT was incubated with 0-10 mM alloxan, and OGT activity was measured directly by quantitating UDP-[(3)H]-GlcNAc incorporation into the recombinant protein substrate, nucleoporin p62.	Alloxan	35-42	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	84-87
12054585-5	2002	In order to show definitively that alloxan was inhibiting OGT activity, recombinant OGT was incubated with 0-10 mM alloxan, and OGT activity was measured directly by quantitating UDP-[(3)H]-GlcNAc incorporation into the recombinant protein substrate, nucleoporin p62.	Alloxan	35-42	nucleoporin 62	Homo sapiens	263-266
12054585-6	2002	Under these conditions, OGT activity was completely inhibited by 1 mM alloxan with half-maximal inhibition achieved at a concentration of 0.1 mM alloxan.	Alloxan	70-77	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	24-27
12054585-6	2002	Under these conditions, OGT activity was completely inhibited by 1 mM alloxan with half-maximal inhibition achieved at a concentration of 0.1 mM alloxan.	Alloxan	145-152	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	24-27
12054585-7	2002	Together, these data demonstrate that alloxan is an inhibitor of OGT, and as such, is the first OGT inhibitor described.	Alloxan	38-45	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	65-68
12054585-7	2002	Together, these data demonstrate that alloxan is an inhibitor of OGT, and as such, is the first OGT inhibitor described.	Alloxan	38-45	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	96-99
11817013-4	2001	Alloxan treatment is associated with a significant increase of thiobarbituric acid reactive substances and the activity of antioxidant enzymes superoxide dismutase and catalase.	Alloxan	0-7	catalase	Rattus norvegicus	168-176
11522665-10	2001	After alloxan administration, insulin secretion and insulin pulse mass (but not insulin pulse interval) decreased in relation to beta-cell mass.	Alloxan	6-13	insulin	Homo sapiens	30-37
11522665-13	2001	We conclude that an alloxan-induced selective decrease in beta-cell mass leads to deficient insulin secretion by attenuating insulin pulse mass, and that the latter is associated with decreased hepatic insulin clearance and relative hyperglucagonemia, thereby emulating the pattern of islet dysfunction observed in type 2 diabetes.	Alloxan	20-27	insulin	Homo sapiens	92-99
11460883-6	2001	NFkappaB activation in the pancreas 30 min after alloxan injection (60 mg/kg, iv), as assessed by an electrophoretic mobility shift assay, was not detected in the mice pretreated with A.	Alloxan	49-56	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	0-8
11510477-4	2001	The formation of DNA ladder was prevented by vitamin E, BHA and catalase, suggesting that the ROS is involved in the process of apoptosis in INS-1 cells treated with alloxan.	Alloxan	166-173	catalase	Rattus norvegicus	45-72
10751203-0	2000	Islet amyloid polypeptide (amylin)-deficient mice develop a more severe form of alloxan-induced diabetes.	Alloxan	80-87	islet amyloid polypeptide	Mus musculus	27-33
10902577-7	2000	Injection of NO in alloxan-induced diabetic mice mimicked the effect of insulin in the control of hyperglycemia (i.e., lowered the glucose content in plasma).	Alloxan	19-26	insulin	Homo sapiens	72-79
11790282-0	2001	Endothelial nitric oxide synthase protein expression, localization, and activity in the penis of the alloxan-induced diabetic rat.	Alloxan	101-108	nitric oxide synthase 3	Rattus norvegicus	0-33
11790282-10	2001	CONCLUSIONS: In the penis of the alloxan-induced diabetic rat, eNOS protein expression and synthetic activity were reduced compared with the normal rat penis, independent of testosterone influence and in the absence of significant erectile tissue degenerative changes.	Alloxan	33-40	nitric oxide synthase 3	Rattus norvegicus	63-67
10700381-4	2000	Controlled proteolysis of wild-type glucokinase by proteinase K revealed that the SH group oxidizing agent alloxan can induce the formation of multiple intramolecular disulfide bridges corresponding to a double-band pattern of glucokinase protein in nonreducing sodium dodecyl sulfate-polyacrylamide gel electrophoresis.	Alloxan	107-114	glucokinase	Homo sapiens	36-47
10700381-4	2000	Controlled proteolysis of wild-type glucokinase by proteinase K revealed that the SH group oxidizing agent alloxan can induce the formation of multiple intramolecular disulfide bridges corresponding to a double-band pattern of glucokinase protein in nonreducing sodium dodecyl sulfate-polyacrylamide gel electrophoresis.	Alloxan	107-114	glucokinase	Homo sapiens	227-238
11053894-3	2000	A single dose of alloxan (100 mg/kg) produced a decrease in insulin level, hyperglycemia, elevated total lipids, triglycerides and cholesterol, decreased high-density lipoprotein and hepatic glycogen contents and elevated hepatic glucose-6-phosphatase activity.	Alloxan	17-24	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	230-251
10868954-4	2000	After a 24-h culture with IL-1beta (30 U/ml), beta-cells exhibited a lower expression of the beta-cell-specific protein transcription factor pancreatic and duodenal homeobox gene (PDX)-1, glucose transporter GLUT2, and proinsulin convertase PC2, with a marked reduction (60-70%) in glucose-induced insulin production and selective sensitivity to the toxins alloxan (ALX) and streptozotocin (STZ).	Alloxan	366-369	interleukin 1 beta	Rattus norvegicus	26-34
10868954-6	2000	This IL-1beta-induced alteration in beta-cell phenotype resulted in a reduced cellular sensitivity to the beta-cell-specific toxins ALX and STZ; the production of nontoxic conditions of nitric oxide (NO) also rendered the cells less susceptible to radical-induced damage.	Alloxan	132-135	interleukin 1 beta	Rattus norvegicus	5-13
10704171-2	2000	The purpose of this study was to determine whether adenovirus-mediated gene transfer of endothelial NO synthase (eNOS) or Cu/Zn superoxide dismutase (SOD1) improves responsiveness to acetylcholine in alloxan-induced diabetic rabbits.	Alloxan	200-207	nitric oxide synthase, endothelial	Oryctolagus cuniculus	113-117
10704171-2	2000	The purpose of this study was to determine whether adenovirus-mediated gene transfer of endothelial NO synthase (eNOS) or Cu/Zn superoxide dismutase (SOD1) improves responsiveness to acetylcholine in alloxan-induced diabetic rabbits.	Alloxan	200-207	superoxide dismutase [Cu-Zn]	Oryctolagus cuniculus	122-148
10628433-6	1999	However, alloxan prevented insulin from increasing (P < 0.001) after feeding (131.8 pmol/1) compared with control steers (442.0 pmol/l) (pooled SEM = 47.5).	Alloxan	9-16	insulin	Homo sapiens	27-34
10765977-6	2000	In the liver phospholipid (PL) fraction, GLA, DGLA (dihomo-GLA) and alpha-linolenic acid (ALA) were decreased in the alloxan-treated group; in the muscle PL fraction, LA, GLA and DGLA were low, whereas an increase in the saturated fatty acid content was noted.	Alloxan	117-124	galactosidase, alpha	Rattus norvegicus	41-44
10765977-6	2000	In the liver phospholipid (PL) fraction, GLA, DGLA (dihomo-GLA) and alpha-linolenic acid (ALA) were decreased in the alloxan-treated group; in the muscle PL fraction, LA, GLA and DGLA were low, whereas an increase in the saturated fatty acid content was noted.	Alloxan	117-124	galactosidase alpha	Homo sapiens	47-50
10765977-6	2000	In the liver phospholipid (PL) fraction, GLA, DGLA (dihomo-GLA) and alpha-linolenic acid (ALA) were decreased in the alloxan-treated group; in the muscle PL fraction, LA, GLA and DGLA were low, whereas an increase in the saturated fatty acid content was noted.	Alloxan	117-124	galactosidase alpha	Homo sapiens	47-50
10765977-7	2000	L-arginine (the precursor of nitric oxide) and sodium nitroprusside (a nitric oxide donor) treatment of alloxan-induced diabetic rats enhanced the levels of LA, GLA and DGLA.	Alloxan	104-111	galactosidase, alpha	Rattus norvegicus	161-164
10535453-10	1999	A dominant genetic trait from ALR/Lt controlling this unusual AL resistance was indicated by the finding that reciprocal F1 mice of both sexes were resistant to AL administration in vivo.	Alloxan	62-64	growth factor, augmenter of liver regeneration	Mus musculus	30-33
11467412-0	2000	Streptozotocin and alloxan-based selection improves toxin resistance of insulin-producing RINm cells.	Alloxan	19-26	insulin	Homo sapiens	72-79
10661714-3	1999	Alloxan elicited significant inhibition of antioxidants including superoxide dismutase, catalase and glutathione reductase activities and decreased glutathione content in testis.	Alloxan	0-7	catalase	Rattus norvegicus	88-96
10661714-3	1999	Alloxan elicited significant inhibition of antioxidants including superoxide dismutase, catalase and glutathione reductase activities and decreased glutathione content in testis.	Alloxan	0-7	glutathione-disulfide reductase	Rattus norvegicus	101-122
9703225-4	1998	Unlike alloxan, alloxan-glutathione (GSH) and dialuric acid increased lipid peroxidation, which could be explained by the decreased activity of catalase and GSH peroxidase during incubation.	Alloxan	16-23	catalase	Rattus norvegicus	144-152
10506589-8	1999	Activation of NFkappaB in pancreatic nuclear extracts was observed 30 min after alloxan injection, as assessed by an electrophoretic mobility shift assay.	Alloxan	80-87	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	14-22
9862424-4	1998	The activities of citrate synthase, malate synthase and malate dehydrogenase detected in the peroxisomal fraction were also increased by alloxan treatment.	Alloxan	137-144	citrate synthase	Rattus norvegicus	18-34
9862424-4	1998	The activities of citrate synthase, malate synthase and malate dehydrogenase detected in the peroxisomal fraction were also increased by alloxan treatment.	Alloxan	137-144	citramalyl-CoA lyase	Rattus norvegicus	36-51
9823015-8	1998	At 6 weeks after alloxan administration, a significant depression of the Na(+)-K+ ATPase alpha 1-subunit mRNA was noted in diabetic heart.	Alloxan	17-24	ATPase Na+/K+ transporting subunit alpha 1	Rattus norvegicus	73-104
9784839-1	1998	Effect of alloxan induced diabetes on the activity of adenosine deaminase (ADA) was studied in the liver, spleen, stomach and small intestine of mice at two different postnatal ages (preweaned, 15-day and postweaned, 60-day).	Alloxan	10-17	adenosine deaminase	Mus musculus	54-73
9784839-1	1998	Effect of alloxan induced diabetes on the activity of adenosine deaminase (ADA) was studied in the liver, spleen, stomach and small intestine of mice at two different postnatal ages (preweaned, 15-day and postweaned, 60-day).	Alloxan	10-17	adenosine deaminase	Mus musculus	75-78
10468221-2	1999	Alloxan-susceptible (ALS/Lt) and AL-resistant (ALR/Lt) are inbred mouse strains derived in Japan by inbreeding CD-1 (ICR) mice with concomitant selection for high or low sensitivity to a relatively low AL dose.	Alloxan	33-35	growth factor, augmenter of liver regeneration	Mus musculus	47-50
10468221-4	1999	Superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), and glutathione peroxidase (GPX) activities were determined in tissues of AL-untreated ALR/Lt and ALS/Lt male mice at 7 weeks of age.	Alloxan	146-148	growth factor, augmenter of liver regeneration	Mus musculus	159-162
9833941-0	1998	Evidence for direct action of alloxan to induce insulin resistance at the cellular level.	Alloxan	30-37	insulin	Canis lupus familiaris	48-55
9833941-6	1998	During clamps, steady state arterial insulin was higher in dogs treated with alloxan (688 +/- 60 vs 502 +/- 38 pmol/l; p = 0.023) due to a 25% reduction in insulin clearance (p = 0.045).	Alloxan	77-84	insulin	Canis lupus familiaris	37-44
9833941-6	1998	During clamps, steady state arterial insulin was higher in dogs treated with alloxan (688 +/- 60 vs 502 +/- 38 pmol/l; p = 0.023) due to a 25% reduction in insulin clearance (p = 0.045).	Alloxan	77-84	insulin	Canis lupus familiaris	156-163
9833941-10	1998	In conclusion, alloxan induces insulinopenic diabetes, with glucose intolerance and insulin resistance at the target tissue level.	Alloxan	15-22	insulin	Canis lupus familiaris	31-38
9048894-6	1997	The human and rat glucokinase isoforms were non-competitively inhibited by the sulfhydryl group reagents alloxan and ninhydrin with Ki values in the range of 1 microM.	Alloxan	105-112	glucokinase	Rattus norvegicus	18-29
9741596-1	1998	Alloxan is known to induce diabetes in experimental animals through destruction of insulin-producing 3-cells of pancreas.	Alloxan	0-7	insulin	Homo sapiens	83-90
9467831-1	1997	The status of cytochrome P450-dependent oxidative biotransformation of aminopyrine and benzo(a)pyrene (Phase I reaction) and glutathione S-transferase (GST) catalyzed conjugation with 1-chloro-2,4-dinitrobenzene (CDNB) (Phase II reaction) was evaluated in diabetic rats sacrificed 3 weeks after alloxan treatment (2 doses of 75 mg/kg at an interval of 48 h, i.p.).	Alloxan	295-302	hematopoietic prostaglandin D synthase	Rattus norvegicus	125-150
9467831-1	1997	The status of cytochrome P450-dependent oxidative biotransformation of aminopyrine and benzo(a)pyrene (Phase I reaction) and glutathione S-transferase (GST) catalyzed conjugation with 1-chloro-2,4-dinitrobenzene (CDNB) (Phase II reaction) was evaluated in diabetic rats sacrificed 3 weeks after alloxan treatment (2 doses of 75 mg/kg at an interval of 48 h, i.p.).	Alloxan	295-302	hematopoietic prostaglandin D synthase	Rattus norvegicus	152-155
9178105-2	1997	The adenylate cyclase inhibitor, alloxan, blocked parathyroid hormone (PTH)-stimulated acid production.	Alloxan	33-40	parathyroid hormone	Gallus gallus	50-69
9450640-1	1997	The effect of alloxan-induced diabetes was studied on the activity of monoamine oxidase (MAO), the oxidative deaminating enzyme of monoamine neurotransmitters.	Alloxan	14-21	monoamine oxidase A	Rattus norvegicus	70-87
9450640-1	1997	The effect of alloxan-induced diabetes was studied on the activity of monoamine oxidase (MAO), the oxidative deaminating enzyme of monoamine neurotransmitters.	Alloxan	14-21	monoamine oxidase A	Rattus norvegicus	89-92
9048894-7	1997	The inhibition of glucokinase enzyme activity was reversed by dithiothreitol with an EC50 value of 9 microM for alloxan and of 50 microM for ninhydrin.	Alloxan	112-119	glucokinase	Homo sapiens	18-29
9048894-8	1997	D-Glucose provided protection against alloxan-induced inhibition of human and rat glucokinase isoenzymes with half-maximal effective concentrations between 11 and 16 mM.	Alloxan	38-45	glucokinase	Rattus norvegicus	82-93
9048894-9	1997	The enzyme inhibition by alloxan was accompanied by a change in the electrophoretic mobility with a second lower molecular 49 kDa glucokinase band which can be interpreted as a compact glucokinase molecule locked by disulfide bonds.	Alloxan	25-32	glucokinase	Homo sapiens	130-141
9048894-9	1997	The enzyme inhibition by alloxan was accompanied by a change in the electrophoretic mobility with a second lower molecular 49 kDa glucokinase band which can be interpreted as a compact glucokinase molecule locked by disulfide bonds.	Alloxan	25-32	glucokinase	Homo sapiens	185-196
9215802-0	1997	Glutathione dependent reduction of alloxan to dialuric acid catalyzed by thioltransferase (glutaredoxin): a possible role for thioltransferase in alloxan toxicity.	Alloxan	35-42	glutaredoxin-1	Sus scrofa	73-89
9215802-0	1997	Glutathione dependent reduction of alloxan to dialuric acid catalyzed by thioltransferase (glutaredoxin): a possible role for thioltransferase in alloxan toxicity.	Alloxan	35-42	glutaredoxin-1	Sus scrofa	91-103
9215802-0	1997	Glutathione dependent reduction of alloxan to dialuric acid catalyzed by thioltransferase (glutaredoxin): a possible role for thioltransferase in alloxan toxicity.	Alloxan	35-42	glutaredoxin-1	Sus scrofa	126-142
9215802-1	1997	Recombinant pig liver thioltransferase (rPLTT) catalyzes the reduction of alloxan to dialuric acid by glutathione (GSH).	Alloxan	74-81	glutaredoxin-1	Sus scrofa	22-38
9215802-5	1997	Both superoxide dismutase and catalase inhibited oxygen consumption in 1.0 mM GSH and 0.2 mM alloxan in the presence of rPLTT.	Alloxan	93-100	catalase	Sus scrofa	30-38
9215802-6	1997	This study suggests that thioltransferase (glutaredoxin) plays a significant role in the cytotoxicity of alloxan in vulnerable tissues.	Alloxan	105-112	glutaredoxin-1	Sus scrofa	25-41
9215802-6	1997	This study suggests that thioltransferase (glutaredoxin) plays a significant role in the cytotoxicity of alloxan in vulnerable tissues.	Alloxan	105-112	glutaredoxin-1	Sus scrofa	43-55
8959353-0	1996	Renal natriuretic effects of atrial natriuretic peptide in dogs with alloxan-induced acute pulmonary edema.	Alloxan	69-76	natriuretic peptide A	Canis lupus familiaris	29-55
8959353-11	1996	Catalase, administered intravenously as a bolus just before the alloxan infusion, prevented pulmonary edema and the associated renal changes.	Alloxan	64-71	catalase	Canis lupus familiaris	0-8
8960250-2	1995	Activity of glutathione S-transferase and glutathione peroxidase in the liver of alloxan induced diabetic rats.	Alloxan	81-88	hematopoietic prostaglandin D synthase	Rattus norvegicus	12-37
27406273-2	1996	The toxic effects are prevented by catalase added to the medium, suggesting that alloxan does not need to be taken up in order to affect cells.	Alloxan	81-88	catalase	Rattus norvegicus	35-43
8161942-0	1994	Effect of alloxan-induced diabetes on acetylcholinesterase activity from discrete areas of rat brain.	Alloxan	10-17	acetylcholinesterase	Rattus norvegicus	38-58
8852272-6	1995	In alloxan-induced diabetes metformin (Met) treatment led to an increase in insulin receptor number in liver plasma membranes (before Met: 46.50 +/- 2.69, after Met: 76.00 +/- 3.39 fmol/mg, p < 0.001) and a decrease in plasma lipid peroxidation levels compared to the non-treated group (before Met: 1.85 +/- 0.53, after Met: 1.10 +/- 0.09 nmol MDA/ml, p < 0.05).	Alloxan	3-10	insulin receptor	Rattus norvegicus	76-92
8159102-2	1994	In the present study, we demonstrate that the mass of HMG CoA reductase protein is increased in the small intestine of both streptozocin-induced diabetic rats (2.5-fold) and streptozocin/alloxan-induced diabetic dogs (2.4-fold).	Alloxan	187-194	3-hydroxy-3-methylglutaryl-CoA reductase	Rattus norvegicus	54-71
7918687-4	1994	Treatment of beta-cells with alloxan and H2O2 caused elevation of cytosolic free Ca2+, and this increase of Ca2+ was also abolished by verapamil.	Alloxan	29-36	carbonic anhydrase 2	Rattus norvegicus	81-84
7918687-4	1994	Treatment of beta-cells with alloxan and H2O2 caused elevation of cytosolic free Ca2+, and this increase of Ca2+ was also abolished by verapamil.	Alloxan	29-36	carbonic anhydrase 2	Rattus norvegicus	108-111
8462284-6	1993	Injection of insulin in alloxan-induced diabetic rats is able to restore almost completely the level of c-Ki-ras transcript found in insulin-induced normal rats.	Alloxan	24-31	KRAS proto-oncogene, GTPase	Rattus norvegicus	104-112
8350431-5	1993	RESULTS: Both insulin-treated and untreated alloxan diabetic rabbits revealed significantly decreased oxygen tensions throughout the arterial wall compared with control rabbits.	Alloxan	44-51	insulin	Oryctolagus cuniculus	14-21
7679153-1	1993	A possible relationship between increased aldose reductase activity and abnormal endothelium-dependent relaxation was examined in aorta from alloxan-induced diabetic rabbits.	Alloxan	141-148	aldo-keto reductase family 1 member B1	Oryctolagus cuniculus	42-58
1606640-0	1992	Enzymatic generation of alloxan radicals in rat liver microsomes: possible participation of reduced nicotinamide adenine dinucleotide phosphate (NADPH)-cytochrome P-450 reductase.	Alloxan	24-31	cytochrome p450 oxidoreductase	Rattus norvegicus	100-178
1638581-5	1992	The alloxan group presented the following significant findings: a decrease in white blood cell and platelet counts (44.2% and 68.2% of control, respectively) at five minutes; an increase in thromboxane B2 and 6-keto-prostaglandin F1 alpha (731.6% and 476.6% of control, respectively) at 15 minutes; an increase in beta-glucuronidase (124.8% of control) at 30 minutes; and an increase in Qwl/dQl (8.84 +/- 1.82 g/g) at the end of experiment.	Alloxan	4-11	glucuronidase beta	Canis lupus familiaris	314-332
1581040-8	1992	Cells pretreated with desferrioxamine (Des) and superoxide dismutase (SOD) or Des, SOD and catalase (CAT) to induce partial (H2O2 formation only) or almost full protection (no ROS formation) showed about the same reactions as when cells were exposed to alloxan and cysteine without scavengers (O2-, H2O2 and OH.	Alloxan	253-260	superoxide dismutase 1	Homo sapiens	48-68
1581040-8	1992	Cells pretreated with desferrioxamine (Des) and superoxide dismutase (SOD) or Des, SOD and catalase (CAT) to induce partial (H2O2 formation only) or almost full protection (no ROS formation) showed about the same reactions as when cells were exposed to alloxan and cysteine without scavengers (O2-, H2O2 and OH.	Alloxan	253-260	superoxide dismutase 1	Homo sapiens	83-86
1581040-8	1992	Cells pretreated with desferrioxamine (Des) and superoxide dismutase (SOD) or Des, SOD and catalase (CAT) to induce partial (H2O2 formation only) or almost full protection (no ROS formation) showed about the same reactions as when cells were exposed to alloxan and cysteine without scavengers (O2-, H2O2 and OH.	Alloxan	253-260	catalase	Homo sapiens	91-99
34511503-9	2021	O-GlcNAc transferase inhibitor alloxan could suppress DHA-induced protein O-GlcNAcylation, and subsequently prevent therapeutic effect of DHA on the deficits of learning and memory as well as synaptic plasticity in hTau mice.	Alloxan	31-38	microtubule associated protein tau	Homo sapiens	215-219
1676625-0	1991	Purification and aminopyrine monooxygenase activity of liver microsomal cytochrome P-450 from alloxan-induced diabetic rats.	Alloxan	94-101	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	72-88
2178745-1	1990	The activity of in vitro glutathione S-transferase towards 1-chloro-2,4-dinitrobenzene was examined in liver, renal cortex, and small intestine (duodenum, jejunum, ileum) after the in vivo treatment of male Wistar rats with streptozotocin or alloxan.	Alloxan	242-249	hematopoietic prostaglandin D synthase	Rattus norvegicus	25-50
34668190-7	2022	Alloxan and Thiamet G were used to reduce and increase global OGT glycosylation levels in C2C12 cells, respectively.	Alloxan	0-7	O-linked N-acetylglucosamine (GlcNAc) transferase (UDP-N-acetylglucosamine:polypeptide-N-acetylglucosaminyl transferase)	Mus musculus	62-65
1284498-3	1992	It is reported that 14 weeks after diabetes induction with alloxan the levels of substance P and methionine-enkephalin are markedly reduced throughout the intestine, while vasoactive intestinal polypeptide content is dramatically increased.	Alloxan	59-66	tachykinin precursor 1	Homo sapiens	81-92
1816091-2	1991	Since a number of central neurotransmitters are also known to influence glucose levels and it is likely that CNS insulin receptors act through neurotransmitter mediation, the present study was conducted to investigate the effect of intracerebroventricularly (icv) administered insulin on rat brain dopamine (DA), noradrenaline (NA), serotonin and acetylcholine (ACh) activity in normal and alloxan-induced hyperglycaemic animals.	Alloxan	390-397	insulin	Homo sapiens	113-120
2205570-2	1990	The insulin level in alloxan-induced hyperglycemic animals increased significantly after treatment with VRV.	Alloxan	21-28	insulin	Oryctolagus cuniculus	4-11
2185463-2	1990	Half maximal inhibitory concentrations of alloxan were greater than those previously found for half maximal inhibition of pancreatic islet or liver glucokinase.	Alloxan	42-49	glucokinase	Rattus norvegicus	148-159
34175449-10	2021	These findings suggest that alloxan might be a better option for animal studies regarding painful diabetic neuropathy as streptozotocin directly affects nociceptive neurons, probably by modulating TRPV1 channel activation.	Alloxan	28-35	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	197-202
34341763-0	2021	Abrus precatorius Leaf Extract Reverses Alloxan/Nicotinamide-Induced Diabetes Mellitus in Rats through Hormonal (Insulin, GLP-1, and Glucagon) and Enzymatic (alpha-Amylase/alpha-Glucosidase) Modulation.	Alloxan	40-47	glucagon	Rattus norvegicus	122-127
34341763-0	2021	Abrus precatorius Leaf Extract Reverses Alloxan/Nicotinamide-Induced Diabetes Mellitus in Rats through Hormonal (Insulin, GLP-1, and Glucagon) and Enzymatic (alpha-Amylase/alpha-Glucosidase) Modulation.	Alloxan	40-47	glucagon	Rattus norvegicus	133-141
34629354-2	2021	The diabetogenic agents, alloxan and streptozotocin, caused DNA strand breaks, which in turn activated poly(ADP-ribose) polymerase/synthetase (PARP) to deplete NAD+, thereby inhibiting islet beta-cell functions such as proinsulin synthesis and ultimately leading to beta-cell necrosis.	Alloxan	25-32	poly(ADP-ribose) polymerase 1	Homo sapiens	103-141
34629354-2	2021	The diabetogenic agents, alloxan and streptozotocin, caused DNA strand breaks, which in turn activated poly(ADP-ribose) polymerase/synthetase (PARP) to deplete NAD+, thereby inhibiting islet beta-cell functions such as proinsulin synthesis and ultimately leading to beta-cell necrosis.	Alloxan	25-32	poly(ADP-ribose) polymerase 1	Homo sapiens	143-147
34629354-2	2021	The diabetogenic agents, alloxan and streptozotocin, caused DNA strand breaks, which in turn activated poly(ADP-ribose) polymerase/synthetase (PARP) to deplete NAD+, thereby inhibiting islet beta-cell functions such as proinsulin synthesis and ultimately leading to beta-cell necrosis.	Alloxan	25-32	insulin	Homo sapiens	219-229
35190649-10	2022	AEPAS showed a marked decrease in alloxan-induced increases in FBG, TG, LDL-c, G6P, F-1, 6-BP, MDA, IL-6, TNF-alpha, and NF-kB and increased alloxan-induced decreases in liver glycogen, hexokinase, and HDL-c.	Alloxan	34-41	interleukin 6	Rattus norvegicus	100-104
35308202-16	2022	Conclusion: AECPS showed efficient ameliorative actions against alloxan-induced pancreatic dysfunction, oxidative stress suppression as well as, inflammation, and apoptosis via the activation of PI3K/AKT signaling pathways.	Alloxan	64-71	AKT serine/threonine kinase 1	Rattus norvegicus	200-203
35190649-10	2022	AEPAS showed a marked decrease in alloxan-induced increases in FBG, TG, LDL-c, G6P, F-1, 6-BP, MDA, IL-6, TNF-alpha, and NF-kB and increased alloxan-induced decreases in liver glycogen, hexokinase, and HDL-c.	Alloxan	34-41	tumor necrosis factor	Rattus norvegicus	106-115
35190649-10	2022	AEPAS showed a marked decrease in alloxan-induced increases in FBG, TG, LDL-c, G6P, F-1, 6-BP, MDA, IL-6, TNF-alpha, and NF-kB and increased alloxan-induced decreases in liver glycogen, hexokinase, and HDL-c.	Alloxan	34-41	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	121-126
2745981-4	1989	Oxidant stress, in the form of alloxan or divicine, also enhanced serum levels of TNF in mice made sensitive to LPS by low-level infection with malaria, and then given i.v.	Alloxan	31-38	tumor necrosis factor	Mus musculus	82-85
34986201-8	2022	Alloxan-diabetic rabbits had lower levels of SOD, CAT, Gpx, and rGSH than control rabbits.	Alloxan	0-7	catalase	Oryctolagus cuniculus	50-53
2471969-4	1989	Injection of alloxan (125 mg/kg) induced a similar change of pancreatic enzyme pattern, with amylase activity strongly reduced by 79% and activity of lipase and colipase increased 20.5 and 18.6%, respectively.	Alloxan	13-20	lipase G, endothelial type	Rattus norvegicus	150-156
2536542-7	1989	In the presence of SOD, alloxan was reduced by GSH, but increasing concentrations of GSH progressively inhibited redox cycling as shown by decreased rates of O2 uptake and GSH oxidation.	Alloxan	24-31	superoxide dismutase 1	Homo sapiens	19-22
2471969-4	1989	Injection of alloxan (125 mg/kg) induced a similar change of pancreatic enzyme pattern, with amylase activity strongly reduced by 79% and activity of lipase and colipase increased 20.5 and 18.6%, respectively.	Alloxan	13-20	colipase	Rattus norvegicus	161-169
2457529-1	1988	Exocrine secretory function in response to 10 pM to 10 nM synthetic secretin was evaluated in perfused pancreas isolated from control, streptozocin-induced diabetic (STZ-D), alloxan-induced diabetic (ALX-D), and insulin-treated STZ-D rats.	Alloxan	174-181	secretin	Rattus norvegicus	68-76
3207996-0	1988	Structural requirements of alloxan and ninhydrin for glucokinase inhibition and of glucose for protection against inhibition.	Alloxan	27-34	glucokinase	Homo sapiens	53-64
3207996-4	1988	With a half-maximal inhibitory concentration of 5 microM, alloxan was the most potent pyrimidine derivative inhibitor of glucokinase.	Alloxan	58-65	glucokinase	Homo sapiens	121-132
3207996-12	1988	Only glucose derivatives with a sufficiently bulky substituent in position C-2, such as the glucokinase substrates glucose and mannose and the inhibitors mannoheptulose, glucosamine, and N-acetylglucosamine, protected glucokinase against inhibition by alloxan by binding to the active site of the enzyme.	Alloxan	252-259	glucokinase	Homo sapiens	92-103
3207996-12	1988	Only glucose derivatives with a sufficiently bulky substituent in position C-2, such as the glucokinase substrates glucose and mannose and the inhibitors mannoheptulose, glucosamine, and N-acetylglucosamine, protected glucokinase against inhibition by alloxan by binding to the active site of the enzyme.	Alloxan	252-259	glucokinase	Homo sapiens	218-229
3207996-15	1988	DTT (dithiothreitol) protected glucokinase against inhibition by alloxan and reversed the inhibition of the enzyme induced by alloxan.	Alloxan	65-72	glucokinase	Homo sapiens	31-42
3207996-16	1988	Thus the mechanism of glucokinase inhibition by alloxan and other inhibitors, such as uramil and ninhydrin, is an oxidation of functionally essential SH groups of the enzyme, where the most reactive keto group of the inhibitor acts as the hydrogen acceptor.	Alloxan	48-55	glucokinase	Homo sapiens	22-33
2968936-1	1988	A common mechanism has been proposed for the beta-cell toxins alloxan (ALX) and streptozocin (STZ) involving the formation of single-strand breaks in DNA that lead to the overactivation of the enzyme poly(ADP-ribose) synthetase and the critical depletion of its substrate NAD.	Alloxan	71-74	poly(ADP-ribose) polymerase 1	Homo sapiens	200-227
3419426-0	1988	Inhibition of glucokinase by alloxan through interaction with SH groups in the sugar-binding site of the enzyme.	Alloxan	29-36	glucokinase	Homo sapiens	14-25
3419426-2	1988	The dithiol 1,4-dithiothreitol (1,4-DTT) protected against and reversed the inhibition of glucokinase by alloxan.	Alloxan	105-112	glucokinase	Homo sapiens	90-101
3077897-1	1988	After intravenous administration of alloxan (50 mg kg-1 liveweight) to lactating ewes, there were triphasic changes in plasma glucose and insulin.	Alloxan	36-43	LOC105613195	Ovis aries	138-145
3419426-4	1988	Only 1,3-dimercaptopropane, 1,4-dimercaptobutane, 1,4-dithioerythritol, and 1,4-DTT, with intermediate spacing between the SH groups, reversed the inhibition of glucokinase induced by alloxan.	Alloxan	184-191	glucokinase	Homo sapiens	161-172
3419426-8	1988	Like alloxan, other dithiol reagents such as ninhydrin, N-ethylmaleimide, and maleimide inhibited glucokinase.	Alloxan	5-12	glucokinase	Homo sapiens	98-109
2465668-8	1988	In rats made diabetic with alloxan or streptozotocin, the B cells were irreversibly damaged and lost both their insulin and IGF-I immunoreactivities, while the IGF-I immunoreactivity was increased in A cells; the D cells remained unchanged.	Alloxan	27-34	insulin-like growth factor 1	Rattus norvegicus	124-129
2465668-8	1988	In rats made diabetic with alloxan or streptozotocin, the B cells were irreversibly damaged and lost both their insulin and IGF-I immunoreactivities, while the IGF-I immunoreactivity was increased in A cells; the D cells remained unchanged.	Alloxan	27-34	insulin-like growth factor 1	Rattus norvegicus	160-165
16414626-2	1988	Diabetiogenic effect of Alloxan was utilized which produced an Insulin-Dependent Diabetic State in the animals.	Alloxan	24-31	insulin	Homo sapiens	63-70
3078228-2	1988	In one study it was found that the diabetes induced by alloxan could be stabilized with exogenous insulin (1.2-1.3 U h-1).	Alloxan	55-62	insulin	Bos taurus	98-105
3298618-1	1987	A combined pharmacokinetic/pharmacodynamic model was proposed to describe the pharmacokinetics of intravenously administered regular insulin (0.55 units/kg) in alloxan-induced diabetic dogs.	Alloxan	160-167	insulin	Canis lupus familiaris	133-140
3153476-1	1987	Cytochrome P450j, an enzyme involved in nitrosamine metabolism, is expressed in hepatic, pulmonary, and renal tissues and its level is elevated in ethanol- and acetone-treated rats as well as in diabetic rats induced by either streptozotocin or alloxan.	Alloxan	245-252	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	0-16
3296598-5	1987	Alloxan inhibited glucokinase but not hexokinase activity in cytoplasmic fractions of pancreatic B-cells and liver.	Alloxan	0-7	glucokinase	Rattus norvegicus	18-29
3296598-7	1987	Glucokinase activity was protected from alloxan toxicity only by D-glucose and D-mannose; the alpha anomer of D-glucose provided significantly greater protection than the beta anomer.	Alloxan	40-47	glucokinase	Rattus norvegicus	0-11
3301234-2	1987	Alloxan induced maternal diabetes (n = 5) associated with fetal hyperglycemia and mild hyperinsulinemia (59.80 +/- 8.10 microU/ml versus a control of 26.25 +/- 3.70, p less than 0.01) increased the insulin receptor number from a control (30 d) of 168 +/- 1.01 to 320 +/- 34 X 10(10)/mg protein (p less than 0.01).	Alloxan	0-7	insulin receptor	Oryctolagus cuniculus	198-214
3829189-0	1986	Inhibition of rat liver glucokinase by alloxan and ninhydrin.	Alloxan	39-46	glucokinase	Rattus norvegicus	24-35
3427902-4	1987	A comparison of cholesterol synthesis and utilization in alloxan-induced diabetic rats and rabbits revealed that interspecies differences existed only in the response of the key enzymes regulating cholesterol utilization, namely cholesterol 7 alpha-hydroxylase and ACAT in the liver and intestine respectively.	Alloxan	57-64	cytochrome P450 7A1	Oryctolagus cuniculus	229-260
3427902-4	1987	A comparison of cholesterol synthesis and utilization in alloxan-induced diabetic rats and rabbits revealed that interspecies differences existed only in the response of the key enzymes regulating cholesterol utilization, namely cholesterol 7 alpha-hydroxylase and ACAT in the liver and intestine respectively.	Alloxan	57-64	sterol O-acyltransferase 1	Oryctolagus cuniculus	265-269
3518714-2	1986	Alloxan-induced maternal diabetes (n = 5) produced mild fetal hyperinsulinemia (D) (plasma insulin concentrations = 59.80 +/- 8.10 microU/ml, control = 26.25 +/- 3.70; p less than 0.01), whereas systemic administration (IMI) of 1.0 U (n = 4) and 2.0 U (n = 4) of insulin to the fetus resulted in moderate (103.13 +/- 34.63 microU/ml) and severe (288.3 +/- 51 microU/ml) fetal hyperinsulinemia respectively.	Alloxan	0-7	insulin	Oryctolagus cuniculus	67-74
3527515-7	1986	In summary, after high doses of alloxan were given guinea pigs, serum insulin levels were reduced below control levels within 24 hr; this was associated with changes in body weight which paralleled changes in insulin levels more closely than did levels of blood or urine glucose; the volume density of immunostained B cells initially decreased and then returned to control levels by 72 hr following alloxan injection.	Alloxan	32-39	insulin	Cavia porcellus	70-77
3527515-7	1986	In summary, after high doses of alloxan were given guinea pigs, serum insulin levels were reduced below control levels within 24 hr; this was associated with changes in body weight which paralleled changes in insulin levels more closely than did levels of blood or urine glucose; the volume density of immunostained B cells initially decreased and then returned to control levels by 72 hr following alloxan injection.	Alloxan	32-39	insulin	Cavia porcellus	209-216
3530846-3	1986	Glucokinase partially purified from transplantable insulinomas or rat liver was inactivated by alloxan with a half-maximal effect at 2-4 microM alloxan.	Alloxan	95-102	glucokinase	Rattus norvegicus	0-11
3518714-2	1986	Alloxan-induced maternal diabetes (n = 5) produced mild fetal hyperinsulinemia (D) (plasma insulin concentrations = 59.80 +/- 8.10 microU/ml, control = 26.25 +/- 3.70; p less than 0.01), whereas systemic administration (IMI) of 1.0 U (n = 4) and 2.0 U (n = 4) of insulin to the fetus resulted in moderate (103.13 +/- 34.63 microU/ml) and severe (288.3 +/- 51 microU/ml) fetal hyperinsulinemia respectively.	Alloxan	0-7	insulin	Oryctolagus cuniculus	91-98
3962581-3	1986	Injection of alloxan resulted in a diabetic state characterized by increased hemoglobin glycosylation, blood and urine glucose and a significant depression of serum insulin levels.	Alloxan	13-20	insulin	Oryctolagus cuniculus	165-172
3158657-3	1985	Alloxan does not inhibit the uptake of Ca2+ but stimulates the release of Ca2+ from liver mitochondria, which is accompanied by oxidation and hydrolysis of pyridine nucleotides.	Alloxan	0-7	carbonic anhydrase 2	Rattus norvegicus	74-77
4080455-1	1985	Diabetes induced by alloxan at day 6 of gestation in Wistar rats produced decreased fetal growth, delayed skeletal ossification, decreased fetal kidney beta-glucuronidase, and an increased frequency of fetal birth defects which correlated with the degree of diabetic control.	Alloxan	20-27	glucuronidase, beta	Rattus norvegicus	152-170
3158657-7	1985	It is concluded that alloxan can cause Ca2+ release from intact rat liver mitochondria.	Alloxan	21-28	carbonic anhydrase 2	Rattus norvegicus	39-42
3158657-9	1985	Oxidation and hydrolysis of pyridine nucleotides, possibly in conjunction with oxidation of critical sulfhydryl groups, seem to be key events in the alloxan-induced Ca2+ release.	Alloxan	149-156	carbonic anhydrase 2	Rattus norvegicus	165-168
6497140-7	1984	Sodium and chloride values were depressed in steers with alloxan-induced diabetes; these values remained significantly (P less than 0.05) lower than base-line values, even in steers given insulin.	Alloxan	57-64	insulin	Homo sapiens	188-195
3883362-1	1985	In insulin-deprived alloxan-induced diabetic dogs with severe hyperglycemia and marked hyperglucagonemia, glucagon was not suppressed by intravenous infusion of glucose at a progressively increasing rate up to 24 mg/kg of body weight per min.	Alloxan	20-27	insulin	Canis lupus familiaris	3-10
6240981-0	1984	Inhibition of glucokinase in hepatocytes by alloxan.	Alloxan	44-51	glucokinase	Rattus norvegicus	14-25
6240981-1	1984	The effect of alloxan on glucokinase in isolated rat hepatocytes was studied.	Alloxan	14-21	glucokinase	Rattus norvegicus	25-36
6240981-2	1984	Exposure of hepatocytes to alloxan (3 mM) at 30 degrees C for 5 min produced a marked inhibition (77%) of glucokinase activity and altered slightly the phosphofructokinase activity (32% inhibition).	Alloxan	27-34	glucokinase	Rattus norvegicus	106-117
6240981-7	1984	These results suggest that alloxan may exert its cytotoxic action through the inhibition of glucokinase activity not only in the liver but also in the pancreatic islets, since liver and islet glucokinases are known to be quite similar in various properties.	Alloxan	27-34	glucokinase	Rattus norvegicus	92-103
6510522-2	1984	The following approximative alloxan concentrations induced 50% inhibition of enzyme activity: 10(-6)M for aconitase, 10(-4)M for NAD-linked isocitrate dehydrogenase, glutamate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinyl-CoA synthetase and fumarase, and 10(-3)M for citrate synthase and NADP-linked isocitrate dehydrogenase.	Alloxan	28-35	oxoglutarate (alpha-ketoglutarate) dehydrogenase (lipoamide)	Mus musculus	191-224
6510522-2	1984	The following approximative alloxan concentrations induced 50% inhibition of enzyme activity: 10(-6)M for aconitase, 10(-4)M for NAD-linked isocitrate dehydrogenase, glutamate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinyl-CoA synthetase and fumarase, and 10(-3)M for citrate synthase and NADP-linked isocitrate dehydrogenase.	Alloxan	28-35	fumarate hydratase 1	Mus musculus	254-262
6510522-2	1984	The following approximative alloxan concentrations induced 50% inhibition of enzyme activity: 10(-6)M for aconitase, 10(-4)M for NAD-linked isocitrate dehydrogenase, glutamate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinyl-CoA synthetase and fumarase, and 10(-3)M for citrate synthase and NADP-linked isocitrate dehydrogenase.	Alloxan	28-35	citrate synthase	Mus musculus	280-296
6237009-3	1984	Exposure of islets to alloxan (2 mM) in vitro caused a marked inhibition of both glucose-stimulated proinsulin biosynthesis and insulin release, and this was not affected by the action of nicotinamide.	Alloxan	22-29	insulin II	Mus musculus	100-110
6237009-10	1984	The inability of nicotinamide to prevent the alloxan-induced impairment of proinsulin biosynthesis, insulin release, and oxygen uptake, together with the failure of nicotinamide to prevent the development of diabetes when given after alloxan, does not support a current hypothesis that the major cytotoxic effect of alloxan is primarily due to DNA damage.	Alloxan	45-52	insulin II	Mus musculus	75-85
6240183-6	1984	The activities of liver beta-glucuronidase, beta-N-acetyl glucosaminidase and cathepsin D were significantly increased in rats treated with streptozotocin and alloxan.	Alloxan	159-166	glucuronidase, beta	Rattus norvegicus	24-42
6351093-5	1983	Furthermore, insulin release from guinea pig but not rat cultures increased transiently at between 6 and 18 hr during the first day following exposure to all doses of alloxan.	Alloxan	167-174	insulin	Cavia porcellus	13-20
6240183-6	1984	The activities of liver beta-glucuronidase, beta-N-acetyl glucosaminidase and cathepsin D were significantly increased in rats treated with streptozotocin and alloxan.	Alloxan	159-166	cathepsin D	Rattus norvegicus	78-89
6363170-1	1984	The pretreatment of isolated islets of Langerhans with concanavalin A (Con A) completely blocks alloxan from suppressing the insulin release response to glucose.	Alloxan	96-103	insulin	Homo sapiens	125-132
6420098-3	1984	Three parameters of cell-mediated immunity, namely, (a) resistance to infection with Candida albicans, (b) in vivo release of migration inhibitory factor (MIF) into the circulation and (c) delayed hypersensitivity were markedly reduced when mice of such normally resistant high responder strains as C57B1/10SNJ and C57B1/KsJ became hyperglycaemic after treatment with alloxan.	Alloxan	368-375	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	155-158
6404681-1	1983	This study examined the effect of an aldose reductase inhibitor (Sorbinil, CP 45634, Pfizer, Sandwich, Kent, United Kingdom) on the metabolite profile of the lens during the first week after induction of diabetes with alloxan.	Alloxan	218-225	aldo-keto reductase family 1 member B1	Rattus norvegicus	37-53
6309589-4	1983	Comparison of the alloxan- or streptozotocin-treated groups with control animals showed an increase in lysosomal enzymes (cathepsin B1, cathepsin D, beta-glucuronidase and beta-N-acetyl glucosaminidase in skin, liver and spleen) (p less than 0.05) but beta-N-acetyl glucosaminidase was unchanged in the spleen of streptozotocin-diabetic rats.	Alloxan	18-25	cathepsin B	Rattus norvegicus	122-134
6309589-4	1983	Comparison of the alloxan- or streptozotocin-treated groups with control animals showed an increase in lysosomal enzymes (cathepsin B1, cathepsin D, beta-glucuronidase and beta-N-acetyl glucosaminidase in skin, liver and spleen) (p less than 0.05) but beta-N-acetyl glucosaminidase was unchanged in the spleen of streptozotocin-diabetic rats.	Alloxan	18-25	cathepsin D	Rattus norvegicus	136-147
6309589-4	1983	Comparison of the alloxan- or streptozotocin-treated groups with control animals showed an increase in lysosomal enzymes (cathepsin B1, cathepsin D, beta-glucuronidase and beta-N-acetyl glucosaminidase in skin, liver and spleen) (p less than 0.05) but beta-N-acetyl glucosaminidase was unchanged in the spleen of streptozotocin-diabetic rats.	Alloxan	18-25	glucuronidase, beta	Rattus norvegicus	149-167
6341516-5	1983	A large surge of insulin release occurred immediately after alloxan administration, which was followed by a decrease in insulin concentrations to subnormal levels in those animals not treated with insulin.	Alloxan	60-67	insulin	Bos taurus	17-24
6341516-5	1983	A large surge of insulin release occurred immediately after alloxan administration, which was followed by a decrease in insulin concentrations to subnormal levels in those animals not treated with insulin.	Alloxan	60-67	insulin	Bos taurus	120-127
6341516-5	1983	A large surge of insulin release occurred immediately after alloxan administration, which was followed by a decrease in insulin concentrations to subnormal levels in those animals not treated with insulin.	Alloxan	60-67	insulin	Bos taurus	120-127
6753106-2	1982	Compared with the controls, the methyl-prednisolone-treated rats had increased fasting levels of serum insulin, blood glucose, and plasma GIP; the alloxan-treated rats had decreased fasting levels of insulin and increased levels of fasting blood glucose and plasma GIP.	Alloxan	147-154	gastric inhibitory polypeptide	Rattus norvegicus	265-268
7042326-1	1982	Noncarbohydrate nutrients such as 2-ketoisocaproate, L-glutamine, L-leucine and its nonmetabolized analog, beta-2-aminobicyclo[2,2,1]heptane-2-carboxylic acid (BCH) were able to mimic, to a limited extent, the protective action of D-glucose against the inhibitory effect of alloxan on glucose-stimulated insulin release.	Alloxan	274-281	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	107-113
7159455-2	1982	At concentrations of 3.5 mM and above, alloxan caused an increase in lactate dehydrogenase (LDH), glutamate-pyruvate transaminase (GPT) and intracellular potassium (K+) leakage, all of which are indices of plasma membrane damage, and decreased the intracellular reduced glutathione content (GSH) of the cells.	Alloxan	39-46	glutamic--pyruvic transaminase	Rattus norvegicus	98-129
7159455-2	1982	At concentrations of 3.5 mM and above, alloxan caused an increase in lactate dehydrogenase (LDH), glutamate-pyruvate transaminase (GPT) and intracellular potassium (K+) leakage, all of which are indices of plasma membrane damage, and decreased the intracellular reduced glutathione content (GSH) of the cells.	Alloxan	39-46	glutamic--pyruvic transaminase	Rattus norvegicus	131-134
6753106-5	1982	The elevated levels of fasting plasma GIP in the diabetic rats treated with methylprednisolone or alloxan may be due to factors regulating the secretion of GIP rather than to changes in the duodenal content of GIP.	Alloxan	98-105	gastric inhibitory polypeptide	Rattus norvegicus	38-41
6753106-5	1982	The elevated levels of fasting plasma GIP in the diabetic rats treated with methylprednisolone or alloxan may be due to factors regulating the secretion of GIP rather than to changes in the duodenal content of GIP.	Alloxan	98-105	gastric inhibitory polypeptide	Rattus norvegicus	156-159
6753106-5	1982	The elevated levels of fasting plasma GIP in the diabetic rats treated with methylprednisolone or alloxan may be due to factors regulating the secretion of GIP rather than to changes in the duodenal content of GIP.	Alloxan	98-105	gastric inhibitory polypeptide	Rattus norvegicus	156-159
6272129-0	1981	Streptozotocin and alloxan induce DNA strand breaks and poly(ADP-ribose) synthetase in pancreatic islets.	Alloxan	19-26	poly(ADP-ribose) polymerase 1	Homo sapiens	56-83
6753105-4	1982	Similarly, treatment with alloxan was followed by decreased fasting levels of serum insulin, by increased fasting levels of blood glucose and plasma GIP, and by an increased GIP release in response to duodenal glucose and amino acids.	Alloxan	26-33	gastric inhibitory polypeptide	Rattus norvegicus	149-152
6753105-4	1982	Similarly, treatment with alloxan was followed by decreased fasting levels of serum insulin, by increased fasting levels of blood glucose and plasma GIP, and by an increased GIP release in response to duodenal glucose and amino acids.	Alloxan	26-33	gastric inhibitory polypeptide	Rattus norvegicus	174-177
6753105-5	1982	The augmented GIP release in response to duodenal instillation of glucose and amino acids both in methylprednisolone-treated rats and in alloxan-treated rats may be explained by an increased absorption of these nutrients owing to an increased Na+ K+ ATPase activity in the intestinal mucosa of corticosteroid- and alloxan-treated rats.	Alloxan	137-144	gastric inhibitory polypeptide	Rattus norvegicus	14-17
7041886-1	1981	Exogenous superoxide dismutase, catalase and scavengers of the hydroxyl radical protect pancreatic-islet cells against the toxic actions of alloxan in vitro [Grankvist et al.	Alloxan	140-147	catalase	Mus musculus	32-40
6933551-5	1980	Thus, alloxan showed an apparent Km of 70 microM in the presence of 3.4 microM E. coli thioredoxin, 0.2 microM thioredoxin reductase, and 0.4 mM NADPH.	Alloxan	6-13	thioredoxin	Bos taurus	87-98
7024025-11	1981	Rapid reduction of alloxan by thioredoxin in the presence of molecular oxygen and NADPH leads to strong chemiluminescence from luminol indicative of an intense radical protection.	Alloxan	19-26	thioredoxin 1	Mus musculus	30-41
7027617-2	1981	The hypoglycemic effect of insulin, included into this complex as compared with free insulin, was increased more than 2-fold when it was tested in animals with stable alloxane diabetes.	Alloxan	167-175	insulin	Homo sapiens	27-34
6933551-5	1980	Thus, alloxan showed an apparent Km of 70 microM in the presence of 3.4 microM E. coli thioredoxin, 0.2 microM thioredoxin reductase, and 0.4 mM NADPH.	Alloxan	6-13	thioredoxin	Bos taurus	111-122
232388-0	1979	Kinetic studies of the blood serum xanthine dehydrogenase inhibition by alloxan (2,4,5,6-tetraoxypyrimidine 5,6-dioxyuracil).	Alloxan	72-79	xanthine dehydrogenase	Homo sapiens	35-57
6248397-3	1980	A single injection of alloxan (65 mg/kg) led, after 6 weeks, to a 40% decrease of testicular LH- and prolactin-receptor levels.	Alloxan	22-29	luteinizing hormone/choriogonadotropin receptor	Rattus norvegicus	93-119
6444670-1	1980	Dopamine-beta-hydroxylase (DBH) activity is increased at least 5-fold in the serum of rats with experimental diabetes produced by Streptozotocin or Alloxan.	Alloxan	148-155	dopamine beta-hydroxylase	Rattus norvegicus	0-25
6444670-1	1980	Dopamine-beta-hydroxylase (DBH) activity is increased at least 5-fold in the serum of rats with experimental diabetes produced by Streptozotocin or Alloxan.	Alloxan	148-155	dopamine beta-hydroxylase	Rattus norvegicus	27-30
7449751-2	1980	Ornithine decarboxylase (L-ornithine carboxylase; EC 4.1.1.17) (ODC) activity falls to approximately 30% of the control value in diabetic rat kidney 4 weeks after induction of diabetes with alloxan.	Alloxan	190-197	ornithine decarboxylase 1	Rattus norvegicus	0-23
7449751-2	1980	Ornithine decarboxylase (L-ornithine carboxylase; EC 4.1.1.17) (ODC) activity falls to approximately 30% of the control value in diabetic rat kidney 4 weeks after induction of diabetes with alloxan.	Alloxan	190-197	ornithine decarboxylase 1	Rattus norvegicus	64-67
40548-0	1979	Superoxide dismutase, catalase and scavengers of hydroxyl radical protect against the toxic action of alloxan on pancreatic islet cells in vitro.	Alloxan	102-109	catalase	Mus musculus	22-30
40548-6	1979	Superoxide dismutase, catalase, dimethyl sulphoxide, benzoate, and mannitol counteracted the effects of alloxan in both cytotoxicity assays.	Alloxan	104-111	catalase	Mus musculus	22-30
294757-1	1979	Xanthine dehydrogenase activity was determined in blood serum of rats in which diabetes had been induced by alloxan administration.	Alloxan	108-115	xanthine dehydrogenase	Rattus norvegicus	0-22
465017-0	1979	Effect of alloxan-induced chronic diabetes on lipid composition and lipoprotein lipase activity of rat lung.	Alloxan	10-17	lipoprotein lipase	Rattus norvegicus	68-86
321126-0	1977	Effect of alloxan on rat pancreatic polypeptide (PP) cells.	Alloxan	10-17	pancreatic polypeptide	Rattus norvegicus	25-47
711132-5	1978	SPX animals contrastingly showed significantly less response to alloxan than did animals of the other two groups.	Alloxan	64-71	spexin hormone	Rattus norvegicus	0-3
676768-2	1978	After treatment of the diabetic goats with insulin for 4--5 days--the last 24 h intravenously--lactose secretion returned to the control values before alloxan administration provided that normoglycemia developed.	Alloxan	151-158	insulin	Capra hircus	43-50
664469-2	1978	In diabetes the activity of these enzymes in rat kidney, as distinct from liver tissue, was not decreased but it was elevated and within 72 hrs after administration of alloxan the activity of glucose-6-phosphate dehydrogenase was increased 2-fold and the activity  of 6-phosphogluconate dehydrogenase was increased by 30% above the normal level.	Alloxan	168-175	glucose-6-phosphate dehydrogenase	Rattus norvegicus	192-225
331860-4	1977	Starved mice injected with DHCC or PTH 10 minutes before alloxan administration exhibited a pronounced second hyperglycemia of long duration, and extensive, selective B-cell necrosis.	Alloxan	57-64	parathyroid hormone	Mus musculus	35-38
186585-8	1976	Dithiobisnitrobenzoic acid and alloxan, inhibitors of adenylate cyclase, impaired neuromuscular transmission and prevented the effects of NaF, but they did not change the responses to dibutyryl cAMP.	Alloxan	31-38	C-X-C motif chemokine ligand 8	Homo sapiens	138-141
608581-2	1977	The activities of these enzymes were increased significantly in the alloxan-treated rats kept in LD (light: darkness) cycles of 10:14 h. Continuous light exposure to diabetic animals appeared to decrease delta5-3beta-HSD and g-6-PDH in comparison to the diabetic rats kept in 10 h illumination.	Alloxan	68-75	glucose-6-phosphate dehydrogenase	Rattus norvegicus	225-232
138586-1	1977	Duodenal calcium absorption and calcium binding protein (CaBP) are depressed in uncontrolled experimental (alloxan and streptozotocin) diabeties in the rat.	Alloxan	107-114	S100 calcium binding protein G	Rattus norvegicus	9-55
138586-1	1977	Duodenal calcium absorption and calcium binding protein (CaBP) are depressed in uncontrolled experimental (alloxan and streptozotocin) diabeties in the rat.	Alloxan	107-114	S100 calcium binding protein G	Rattus norvegicus	57-61
4278073-0	1974	Effect of insulin infusions on the glucose kinetics in alloxan-steptozotocin diabetic dogs.	Alloxan	55-62	insulin	Canis lupus familiaris	10-17
128691-0	1975	Inhibition of insulin biosynthesis by alloxan, streptozotocin, and N-nitrosomethylurea.	Alloxan	38-45	insulin	Homo sapiens	14-21
164533-1	1975	Studies were performed to examine the effects of alloxan- or streptozotocin-induced diabetes on carbon tetrachloride (CCl4) liver injury.	Alloxan	49-56	C-C motif chemokine ligand 4	Rattus norvegicus	118-122
164533-12	1975	Insulin treatment of rats given alloxan (80 mg/kg) markedly protected against CCl4-induced hepatotoxicity.	Alloxan	32-39	C-C motif chemokine ligand 4	Rattus norvegicus	78-82
5599806-0	1967	[Glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activity in epididymal adipose tissue from normal rats, fasted rats and rats with alloxan-induced diabetes].	Alloxan	154-161	glucose-6-phosphate dehydrogenase	Rattus norvegicus	1-34
4588113-0	1973	Acute effects of alloxan on the metabolism and insulin secretion of the pancreatic B-cell.	Alloxan	17-24	insulin	Homo sapiens	47-54
24683634-1	1972	The extremely high levels of glucagon recently observed in dogs with severe alloxan-induced diabetes decline promptly and precipitously to normal as soon as exogenous insulin is infused.	Alloxan	76-83	insulin	Canis lupus familiaris	167-174
4311516-0	1968	Nature of the increase in liver microsomal glucose-6-phosphatase activity during the early stages of alloxan-induced diabetes.	Alloxan	101-108	glucose-6-phosphatase catalytic subunit 1	Homo sapiens	43-64
4590866-0	1973	[Effect of alloxan on the content of insulin and zinc in the pancreatic islets in experimental animals].	Alloxan	11-18	insulin	Homo sapiens	37-44
4248447-0	1970	C14-proline metabolism in alloxan treated rats.	Alloxan	26-33	anti-Mullerian hormone receptor type 2	Rattus norvegicus	0-3
13792172-2	1959	after the maintenance dose of insulin (28.1%+/-2.9 s.e) in rabbits made severely diabetic with alloxan was significantly different from the change in the blood sugar with the same drug given 72 hr.	Alloxan	95-102	insulin	Oryctolagus cuniculus	30-37
13800358-0	1959	Inhibition of liver hexokinase by dehydroascorbic acid and alloxan.	Alloxan	59-66	hexokinase 1	Homo sapiens	20-30
13886629-0	1962	Effect of alloxan on the insulin content of micro-dissected mammalian pancreatic islets.	Alloxan	10-17	insulin	Homo sapiens	25-32
13463225-0	1957	The preventive effect of glucagon (HGF) against the diabetogenic action of alloxan and its antagonism by insulin.	Alloxan	75-82	hepatocyte growth factor	Homo sapiens	35-38
13544948-0	1958	[Studies on the reduction of alloxan and the oxidation of dialuric acid in the presence of alcohol dehydrogenase].	Alloxan	29-36	aldo-keto reductase family 1 member A1	Homo sapiens	91-112
20286883-0	1946	Effect of alloxan on insulin.	Alloxan	10-17	insulin	Homo sapiens	21-28
14790813-0	1950	Oxidation of uric acid and of alloxan by cytochrome c.	Alloxan	30-37	cytochrome c, somatic	Homo sapiens	41-53
13201714-5	1954	It was therefore concluded that the inhibitory phenomenon was not due to the injection of alloxan per se but that it was associated with one or more factors that characterize the alloxan diabetic state in the rabbit and that are reversible by insulin therapy.	Alloxan	179-186	insulin	Oryctolagus cuniculus	243-250
33470760-10	2021	It is worth noting that the expression of HSP70 and the protein O-GlcNAc modification levels in the Gln-treated group were significantly elevated than the levels in the sepsis group (P < 0.05), and reversed by pretreatment with the HSP and O-GlcNAc inhibitors quercetion and alloxan.	Alloxan	275-282	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	42-47
14839139-0	1950	[Action of the alloxan-dialuric acid system on the activity of cholinesterase in vitro and in vivo].	Alloxan	15-22	butyrylcholinesterase	Homo sapiens	63-77
34015900-8	2021	Interestingly, compared with normal control levels, S1P/EDG-5 was increased in both alloxan and glucose treated pancreatic beta cell than normal control.	Alloxan	84-91	sphingosine-1-phosphate receptor 2	Mus musculus	56-61
34015900-9	2021	MAPK-ERK inhibition strongly decreased the expression of insulin and S1P in glucose- or alloxan-treated RIN-5F cells.	Alloxan	88-95	mitogen-activated protein kinase 1	Mus musculus	5-8
32911700-1	2020	In our study, we aimed to evaluate the effects of Moringa oleifera leaves extract on rat paraoxonase 1 (rPON1) and catalase (rCAT) activities in alloxan-induced diabetic rats.	Alloxan	145-152	paraoxonase 1	Rattus norvegicus	89-102
33039567-6	2021	Results of the mitotic-index observed from the PG-pre-treated-alloxan-administered (PG+ALX) mice group revealed a significant reduction in chromosomal-anomaly, DNA-damage, and an upregulation of the p53 and PARP protein expression when compared to the ALX-treated mice group.	Alloxan	62-69	transformation related protein 53, pseudogene	Mus musculus	199-202
33039567-6	2021	Results of the mitotic-index observed from the PG-pre-treated-alloxan-administered (PG+ALX) mice group revealed a significant reduction in chromosomal-anomaly, DNA-damage, and an upregulation of the p53 and PARP protein expression when compared to the ALX-treated mice group.	Alloxan	62-69	poly (ADP-ribose) polymerase family, member 1	Mus musculus	207-211
32534114-22	2020	RESULTS: Alloxan treatment increased the levels of FBG, total cholesterol, LDL-cholesterol, VLDL-cholesterol, urine ketone and cardiac function indices and reduced the levels of globulin, albumin, HDL-cholesterol, globulin, liver glycogen, hexokinase and glucose-6-phosphate dehydrogenase activities.	Alloxan	9-16	glucose-6-phosphate dehydrogenase	Rattus norvegicus	255-288
32440769-0	2020	Pyrrolidine dithiocarbamate reduces alloxan-induced kidney damage by decreasing nox4, inducible nitric oxide synthase, and metalloproteinase-2.	Alloxan	36-43	NADPH oxidase 4	Rattus norvegicus	80-84
32440769-0	2020	Pyrrolidine dithiocarbamate reduces alloxan-induced kidney damage by decreasing nox4, inducible nitric oxide synthase, and metalloproteinase-2.	Alloxan	36-43	nitric oxide synthase 2	Rattus norvegicus	86-117
33359794-6	2021	More importantly, the protective effects of G-Rh4 on alloxan-induced upregulation of Nrf2 target gene and insulin secretion were abolished by Nrf2 knockdown.	Alloxan	53-60	nuclear factor, erythroid derived 2, like 2	Mus musculus	85-89
33359794-6	2021	More importantly, the protective effects of G-Rh4 on alloxan-induced upregulation of Nrf2 target gene and insulin secretion were abolished by Nrf2 knockdown.	Alloxan	53-60	nuclear factor, erythroid derived 2, like 2	Mus musculus	142-146
32979266-4	2020	Insulin-dependent diabetes was induced by alloxan in female rabbits.	Alloxan	42-49	insulin	Oryctolagus cuniculus	0-7
32911700-1	2020	In our study, we aimed to evaluate the effects of Moringa oleifera leaves extract on rat paraoxonase 1 (rPON1) and catalase (rCAT) activities in alloxan-induced diabetic rats.	Alloxan	145-152	paraoxonase 1	Rattus norvegicus	104-109
32908936-0	2020	Peroxiredoxin 6 Attenuates Alloxan-Induced Type 1 Diabetes Mellitus in Mice and Cytokine-Induced Cytotoxicity in RIN-m5F Beta Cells.	Alloxan	27-34	peroxiredoxin 6	Mus musculus	0-15
32954201-1	2020	Alloxan (AL) is a toxic glucose analogue that acts as a potent diabetogenic inducer by selectively destroying the insulin-producing beta-cells of the pancreas.	Alloxan	0-7	insulin	Homo sapiens	114-121
32954201-1	2020	Alloxan (AL) is a toxic glucose analogue that acts as a potent diabetogenic inducer by selectively destroying the insulin-producing beta-cells of the pancreas.	Alloxan	9-11	insulin	Homo sapiens	114-121
32908936-5	2020	It was shown that PRDX6 prevented hyperglycemia, lowered the mortality rate, restored the plasma cytokine profile, reversed the splenic cell apoptosis, and reduced the beta cell destruction in Langerhans islets in mice with a severe form of alloxan-induced diabetes.	Alloxan	241-248	peroxiredoxin 6	Mus musculus	18-23
32422500-0	2020	Polysaccharides from Opuntia milpa alta alleviate alloxan-induced INS-1 cells apoptosis via reducing oxidative stress and upregulating Nrf2 expression.	Alloxan	50-57	NFE2 like bZIP transcription factor 2	Rattus norvegicus	135-139
32454931-0	2020	Mulberry Fruit Prevents Diabetes and Diabetic Dementia by Regulation of Blood Glucose through Upregulation of Antioxidative Activities and CREB/BDNF Pathway in Alloxan-Induced Diabetic Mice.	Alloxan	160-167	cAMP responsive element binding protein 1	Mus musculus	139-143
32454931-0	2020	Mulberry Fruit Prevents Diabetes and Diabetic Dementia by Regulation of Blood Glucose through Upregulation of Antioxidative Activities and CREB/BDNF Pathway in Alloxan-Induced Diabetic Mice.	Alloxan	160-167	brain derived neurotrophic factor	Mus musculus	144-148
32422500-7	2020	We found that MAPs could attenuate alloxan-induced apoptosis by increasing the expression of Bcl-2 and decreasing the expression of Bax and the activities of caspase-3 and caspase-9.	Alloxan	35-42	BCL2, apoptosis regulator	Rattus norvegicus	93-98
32422500-7	2020	We found that MAPs could attenuate alloxan-induced apoptosis by increasing the expression of Bcl-2 and decreasing the expression of Bax and the activities of caspase-3 and caspase-9.	Alloxan	35-42	BCL2 associated X, apoptosis regulator	Rattus norvegicus	132-135
32422500-7	2020	We found that MAPs could attenuate alloxan-induced apoptosis by increasing the expression of Bcl-2 and decreasing the expression of Bax and the activities of caspase-3 and caspase-9.	Alloxan	35-42	caspase 3	Rattus norvegicus	158-167
32422500-7	2020	We found that MAPs could attenuate alloxan-induced apoptosis by increasing the expression of Bcl-2 and decreasing the expression of Bax and the activities of caspase-3 and caspase-9.	Alloxan	35-42	caspase 9	Rattus norvegicus	172-181
32422500-9	2020	These findings indicated that MAPs could alleviate alloxan-induced beta-cell apoptosis by reducing oxidative stress and upregulating Nrf2 expression.	Alloxan	51-58	NFE2 like bZIP transcription factor 2	Rattus norvegicus	133-137
31637753-0	2019	Tlr1-13, Nod1/2 and antimicrobial gene expression in the epididymis and testis of rats with alloxan-induced diabetes.	Alloxan	92-99	toll-like receptor 1	Rattus norvegicus	0-4
33728270-2	2021	To this end, the antidiabetic activity of aqueous stem-bark extract of A. polycarpa (APE) in alloxan-induced diabetic ICR mice was investigated.	Alloxan	93-100	apurinic/apyrimidinic endonuclease 1	Mus musculus	85-88
32019238-3	2020	Insulin-dependent diabetes was induced by alloxan treatment in female rabbits 10 days before mating.	Alloxan	42-49	insulin	Oryctolagus cuniculus	0-7
31823816-6	2019	RESULTS: BDNF, LXA4 and AA, EPA and DHA protected (P &lt; 0.001 and P &lt; 0.01 respectively) against AL/STZ/DB/BP-induced toxicity to RIN5F cells in vitro.	Alloxan	102-104	brain derived neurotrophic factor	Mus musculus	9-13
31823816-7	2019	AL/ STZ/DB/BP inhibited BDNF and LXA4 production by RIN5F cells and were restored to normal by AA, EPA and DHA.	Alloxan	0-2	brain derived neurotrophic factor	Mus musculus	24-28
31823816-8	2019	Sub-optimal doses of BDNF, LXA4, AA and EPA when used in combination protected against cytotoxic action of AL/STZ/DB/BP on RIN5F cells in vitro by restoring LXA4/BDNF levels and altered antioxidant/lipid peroxides/NO levels (P &lt; 0.01) to normal.	Alloxan	107-109	brain derived neurotrophic factor	Mus musculus	21-25
31823816-8	2019	Sub-optimal doses of BDNF, LXA4, AA and EPA when used in combination protected against cytotoxic action of AL/STZ/DB/BP on RIN5F cells in vitro by restoring LXA4/BDNF levels and altered antioxidant/lipid peroxides/NO levels (P &lt; 0.01) to normal.	Alloxan	107-109	brain derived neurotrophic factor	Mus musculus	162-166
31823816-10	2019	DISCUSSION: AL/STZ/DB/BP-induced cytotoxicity to RIN5F cells in vitro can be prevented by BDNF, LXA4 and AA.	Alloxan	12-14	brain derived neurotrophic factor	Mus musculus	90-94
31823816-11	2019	AL/STZ/DB/BP are cytotoxic, possibly, by suppressing the production of LXA4 and BDNF in RIN5F cells.	Alloxan	0-2	brain derived neurotrophic factor	Mus musculus	80-84
32256963-0	2020	Effect of Caesalpinia bonduc Polyphenol Extract on Alloxan-Induced Diabetic Rats in Attenuating Hyperglycemia by Upregulating Insulin Secretion and Inhibiting JNK Signaling Pathway.	Alloxan	51-58	mitogen-activated protein kinase 8	Rattus norvegicus	159-162
31738423-6	2020	Fluorescence microscopy revealed that alloxan interferes with the motility of cellular organelles (peroxisomes, endosomes and the endoplasmic reticulum) and the pathogen-triggered redistribution of the PEN1/SYP121 t-SNARE protein.	Alloxan	38-45	pentacyclic triterpene synthase 1	Arabidopsis thaliana	202-206
31738423-6	2020	Fluorescence microscopy revealed that alloxan interferes with the motility of cellular organelles (peroxisomes, endosomes and the endoplasmic reticulum) and the pathogen-triggered redistribution of the PEN1/SYP121 t-SNARE protein.	Alloxan	38-45	syntaxin of plants 121	Arabidopsis thaliana	207-213
31378691-8	2020	CONCLUSIONS: Instant tea and matcha supplementation had beneficial effects on regulation of blood glucose and gut microbiota, reversing the changes in microbiota caused by alloxan injection.	Alloxan	172-179	solute carrier family 7 (cationic amino acid transporter, y+ system), member 2	Mus musculus	21-24
32155637-4	2020	OBJECTIVES: We investigated herein the expression and role of semaphorin-3A in the migratory responses of thymocytes from alloxan-induced diabetic mice.	Alloxan	122-129	sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3A	Mus musculus	62-75
30465800-5	2019	Alloxan-induced diabetic wild- type mice (diabetic) developed wounds that were difficult to heal, differently from CCR4-/- diabetic mice (CCR4-/- diabetic), and also from anti-CCL17/22 or anti-CD25-injected diabetic mice that presented with accelerated wound healing and fewer regulatory T cells in the wound bed.	Alloxan	0-7	chemokine (C-C motif) receptor 4	Mus musculus	115-119
31827688-3	2019	Here, we report that increased O-GlcNAcylation by the suppression of OGA activity using thiamet-G and OGA siRNA did not affect autophagy, whereas decreased O-GlcNAcylation caused by OGT inhibition by alloxan and OGT siRNA increased autophagy.	Alloxan	200-207	O-linked N-acetylglucosamine (GlcNAc) transferase (UDP-N-acetylglucosamine:polypeptide-N-acetylglucosaminyl transferase)	Mus musculus	182-185
31827688-6	2019	Additionally, decreasing O-GlcNAcylation by treatment with alloxan, OGT siRNA, and OGA overexpression significantly decreased the level of autophagy substrate SQSTM1/p62, indicating that autophagic degradation was activated.	Alloxan	59-66	sequestosome 1	Mus musculus	159-165
31827688-6	2019	Additionally, decreasing O-GlcNAcylation by treatment with alloxan, OGT siRNA, and OGA overexpression significantly decreased the level of autophagy substrate SQSTM1/p62, indicating that autophagic degradation was activated.	Alloxan	59-66	sequestosome 1	Mus musculus	166-169
30465800-5	2019	Alloxan-induced diabetic wild- type mice (diabetic) developed wounds that were difficult to heal, differently from CCR4-/- diabetic mice (CCR4-/- diabetic), and also from anti-CCL17/22 or anti-CD25-injected diabetic mice that presented with accelerated wound healing and fewer regulatory T cells in the wound bed.	Alloxan	0-7	interleukin 2 receptor, alpha chain	Mus musculus	193-197
30465800-5	2019	Alloxan-induced diabetic wild- type mice (diabetic) developed wounds that were difficult to heal, differently from CCR4-/- diabetic mice (CCR4-/- diabetic), and also from anti-CCL17/22 or anti-CD25-injected diabetic mice that presented with accelerated wound healing and fewer regulatory T cells in the wound bed.	Alloxan	0-7	chemokine (C-C motif) ligand 17	Mus musculus	176-184
30841444-0	2019	Antidiabetic role of a novel protein from garlic via NO in expression of Glut-4/insulin in liver of alloxan induced diabetic mice.	Alloxan	100-107	solute carrier family 2 (facilitated glucose transporter), member 4	Mus musculus	73-79
30894246-9	2019	However, compared with adult pigs, juvenile swine exhibited greater insulin response recovery (complete or partial restoration of peripheral insulin levels to reference values) at 6 mo after alloxan administration.	Alloxan	191-198	insulin	Sus scrofa	68-75
30894246-10	2019	Overall, these results indicate that youth can confer some protection against the diabetogenic effects of alloxan in swine, potentially due in part to the greater insulin response recovery of young pigs.	Alloxan	106-113	insulin	Sus scrofa	163-170
30181664-4	2018	METHODS: The decrease of O-GlcNAcylation by alloxan, an OGT inhibitor, and increase by NAG-thiazolines (NAG-Ae), an O-GlcNAcase inhibitor were tested to investigate the effects of O-GlcNAc alteration on AD like neurodegeneration in SK-N-SH cells.	Alloxan	44-51	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	56-59
30532634-13	2018	According to our findings we confirmed that zingerone restrained the alloxan induced oxidative stress by increasing the activity of reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and reducing the peroxidative damage.	Alloxan	69-76	catalase	Homo sapiens	187-195
30532634-13	2018	According to our findings we confirmed that zingerone restrained the alloxan induced oxidative stress by increasing the activity of reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and reducing the peroxidative damage.	Alloxan	69-76	catalase	Homo sapiens	197-200
29421520-3	2018	hMSC-TERT supported survival of cocultured INS-1E beta-cells during cellular stress by alloxan (ALX) and streptozotocin (STZ), but not in response to IL-1beta.	Alloxan	87-94	telomerase reverse transcriptase	Rattus norvegicus	5-9
29421520-3	2018	hMSC-TERT supported survival of cocultured INS-1E beta-cells during cellular stress by alloxan (ALX) and streptozotocin (STZ), but not in response to IL-1beta.	Alloxan	87-94	insulin 1	Rattus norvegicus	43-48
29421520-3	2018	hMSC-TERT supported survival of cocultured INS-1E beta-cells during cellular stress by alloxan (ALX) and streptozotocin (STZ), but not in response to IL-1beta.	Alloxan	96-99	telomerase reverse transcriptase	Rattus norvegicus	5-9
29421520-3	2018	hMSC-TERT supported survival of cocultured INS-1E beta-cells during cellular stress by alloxan (ALX) and streptozotocin (STZ), but not in response to IL-1beta.	Alloxan	96-99	insulin 1	Rattus norvegicus	43-48
30016155-5	2018	Furthermore, NLRP3 and ASC-deficient mice were protected against oxidative stress-induced diabetes caused by repetitive low-dose alloxan administration, and this was associated with reduced beta-cell death and reduced macrophage infiltration.	Alloxan	129-136	NLR family, pyrin domain containing 3	Mus musculus	13-18
30181664-4	2018	METHODS: The decrease of O-GlcNAcylation by alloxan, an OGT inhibitor, and increase by NAG-thiazolines (NAG-Ae), an O-GlcNAcase inhibitor were tested to investigate the effects of O-GlcNAc alteration on AD like neurodegeneration in SK-N-SH cells.	Alloxan	44-51	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	25-33
29784660-5	2018	beta-Cell-specific loss of IL-6 signaling in vivo renders mice more susceptible to oxidative damage and cell death through the selective beta-cell toxins streptozotocin and alloxan.	Alloxan	173-180	interleukin 6	Homo sapiens	27-31
29929439-7	2018	In contrast, cyclin-B1 and cyclin-dependent kinase 1, mediators of G2 arrest, were remarkably changed in ALX-treated rats.	Alloxan	105-108	cyclin B1	Rattus norvegicus	13-22
29929439-7	2018	In contrast, cyclin-B1 and cyclin-dependent kinase 1, mediators of G2 arrest, were remarkably changed in ALX-treated rats.	Alloxan	105-108	cyclin-dependent kinase 1	Rattus norvegicus	27-52
29929439-9	2018	Moreover, heat-shock 70 kDA protein 1A ( Hspa1a), Hsp90ab1, and Hsph1 were upregulated in ALX-treated rats, suggesting that ALX treatment injures beta cells via endoplasmic reticulum stress.	Alloxan	90-93	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	10-38
29929439-9	2018	Moreover, heat-shock 70 kDA protein 1A ( Hspa1a), Hsp90ab1, and Hsph1 were upregulated in ALX-treated rats, suggesting that ALX treatment injures beta cells via endoplasmic reticulum stress.	Alloxan	90-93	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	41-47
29929439-9	2018	Moreover, heat-shock 70 kDA protein 1A ( Hspa1a), Hsp90ab1, and Hsph1 were upregulated in ALX-treated rats, suggesting that ALX treatment injures beta cells via endoplasmic reticulum stress.	Alloxan	90-93	heat shock protein 90 alpha family class B member 1	Rattus norvegicus	50-58
29929439-9	2018	Moreover, heat-shock 70 kDA protein 1A ( Hspa1a), Hsp90ab1, and Hsph1 were upregulated in ALX-treated rats, suggesting that ALX treatment injures beta cells via endoplasmic reticulum stress.	Alloxan	90-93	heat shock protein family H (Hsp110) member 1	Rattus norvegicus	64-69
29929439-9	2018	Moreover, heat-shock 70 kDA protein 1A ( Hspa1a), Hsp90ab1, and Hsph1 were upregulated in ALX-treated rats, suggesting that ALX treatment injures beta cells via endoplasmic reticulum stress.	Alloxan	124-127	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	10-38
29929439-9	2018	Moreover, heat-shock 70 kDA protein 1A ( Hspa1a), Hsp90ab1, and Hsph1 were upregulated in ALX-treated rats, suggesting that ALX treatment injures beta cells via endoplasmic reticulum stress.	Alloxan	124-127	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	41-47
29929439-9	2018	Moreover, heat-shock 70 kDA protein 1A ( Hspa1a), Hsp90ab1, and Hsph1 were upregulated in ALX-treated rats, suggesting that ALX treatment injures beta cells via endoplasmic reticulum stress.	Alloxan	124-127	heat shock protein 90 alpha family class B member 1	Rattus norvegicus	50-58
29929439-9	2018	Moreover, heat-shock 70 kDA protein 1A ( Hspa1a), Hsp90ab1, and Hsph1 were upregulated in ALX-treated rats, suggesting that ALX treatment injures beta cells via endoplasmic reticulum stress.	Alloxan	124-127	heat shock protein family H (Hsp110) member 1	Rattus norvegicus	64-69