PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27137793-1 2016 BACKGROUND: Intracellular antioxidant response to high glucose is mediated by Cu/Mn-superoxide dismutases (SOD-1/SOD-2), catalase (CAT) and glutathione peroxidases (GPx), particularly glutathione peroxidase-1 (GPx-1). Glucose 55-62 superoxide dismutase 1 Homo sapiens 107-112 27236050-3 2016 Some of ALS-related genes such as TARDBP or SOD1 among others have important roles in the regulation of glucose and fatty acids metabolism, so that an impairment of fatty acids (FA) consumption and ketogenic deficits during exercise in ALS patients would connect the physiopathology with some of the more intriguing epidemiological traits of the disease. Glucose 104-111 superoxide dismutase 1 Homo sapiens 8-11 27236050-3 2016 Some of ALS-related genes such as TARDBP or SOD1 among others have important roles in the regulation of glucose and fatty acids metabolism, so that an impairment of fatty acids (FA) consumption and ketogenic deficits during exercise in ALS patients would connect the physiopathology with some of the more intriguing epidemiological traits of the disease. Glucose 104-111 superoxide dismutase 1 Homo sapiens 44-48 27236050-3 2016 Some of ALS-related genes such as TARDBP or SOD1 among others have important roles in the regulation of glucose and fatty acids metabolism, so that an impairment of fatty acids (FA) consumption and ketogenic deficits during exercise in ALS patients would connect the physiopathology with some of the more intriguing epidemiological traits of the disease. Glucose 104-111 superoxide dismutase 1 Homo sapiens 236-239 27137793-9 2016 RESULTS: After exposure to constant high glucose SOD-1 and GPx-1 increased, while in oscillating glucose SOD-1 increased and GPx-1 did not. Glucose 41-48 superoxide dismutase 1 Homo sapiens 49-54 25148264-3 2015 Coincubation of endothelial cells with high glucose for 6, 12, 24 and 48 h resulted in a significant decrease in NCX expression, superoxide dismutase (SOD) activity and the release of nitric oxide (NO), and increased NCX activity and malondialdehyde (MDA) production. Glucose 44-51 superoxide dismutase 1 Homo sapiens 129-149 25516495-5 2015 Overexpression of the antioxidant enzyme, superoxide dismutase 1 (SOD1), or treatment with the SOD1 mimetic Tempol, abolished the effect of maternal diabetes or high glucose on miR-322 and TRAF3 expression, respectively. Glucose 166-173 superoxide dismutase 1 Homo sapiens 42-64 25516495-5 2015 Overexpression of the antioxidant enzyme, superoxide dismutase 1 (SOD1), or treatment with the SOD1 mimetic Tempol, abolished the effect of maternal diabetes or high glucose on miR-322 and TRAF3 expression, respectively. Glucose 166-173 superoxide dismutase 1 Homo sapiens 66-70 25516495-5 2015 Overexpression of the antioxidant enzyme, superoxide dismutase 1 (SOD1), or treatment with the SOD1 mimetic Tempol, abolished the effect of maternal diabetes or high glucose on miR-322 and TRAF3 expression, respectively. Glucose 166-173 superoxide dismutase 1 Homo sapiens 95-99 25148264-3 2015 Coincubation of endothelial cells with high glucose for 6, 12, 24 and 48 h resulted in a significant decrease in NCX expression, superoxide dismutase (SOD) activity and the release of nitric oxide (NO), and increased NCX activity and malondialdehyde (MDA) production. Glucose 44-51 superoxide dismutase 1 Homo sapiens 151-154 23332757-0 2013 SOD1 integrates signals from oxygen and glucose to repress respiration. Glucose 40-47 superoxide dismutase 1 Homo sapiens 0-4 24590293-8 2014 The changes of SOD and MDA level in high glucose-treated HUVECs were also prevented by Neferine. Glucose 41-48 superoxide dismutase 1 Homo sapiens 15-18 24997046-3 2014 Addition of SOD to the medium inhibited LDL oxidation, indicating the formation of superoxide anion-radicals under autoxidation of glucose. Glucose 131-138 superoxide dismutase 1 Homo sapiens 12-15 24997046-4 2014 Similarly, SOD inhibited free radical peroxidation of liposomes from egg lecithin in the presence of glucose that confirms the generation of superoxide radicals under co-oxidation of unsaturated lipids and glucose. Glucose 101-108 superoxide dismutase 1 Homo sapiens 11-14 24997046-4 2014 Similarly, SOD inhibited free radical peroxidation of liposomes from egg lecithin in the presence of glucose that confirms the generation of superoxide radicals under co-oxidation of unsaturated lipids and glucose. Glucose 206-213 superoxide dismutase 1 Homo sapiens 11-14 24412154-5 2014 Therefore, the glycation of SOD by glucose or methylglyoxal (MG) and its protection by TQ has been investigated. Glucose 35-42 superoxide dismutase 1 Homo sapiens 28-31 24412154-6 2014 Incubation of SOD with glucose, MG or both at 37 C resulted in a progressive decrease in the activity of the enzyme, and a parallel decrease in the amount of protein on SDS-PAGE gels for glucose incubated SOD and formation of high molecular weight aggregates for MG or both glucose and MG incubated enzyme. Glucose 23-30 superoxide dismutase 1 Homo sapiens 14-17 24412154-6 2014 Incubation of SOD with glucose, MG or both at 37 C resulted in a progressive decrease in the activity of the enzyme, and a parallel decrease in the amount of protein on SDS-PAGE gels for glucose incubated SOD and formation of high molecular weight aggregates for MG or both glucose and MG incubated enzyme. Glucose 23-30 superoxide dismutase 1 Homo sapiens 206-209 24412154-6 2014 Incubation of SOD with glucose, MG or both at 37 C resulted in a progressive decrease in the activity of the enzyme, and a parallel decrease in the amount of protein on SDS-PAGE gels for glucose incubated SOD and formation of high molecular weight aggregates for MG or both glucose and MG incubated enzyme. Glucose 188-195 superoxide dismutase 1 Homo sapiens 14-17 24412154-6 2014 Incubation of SOD with glucose, MG or both at 37 C resulted in a progressive decrease in the activity of the enzyme, and a parallel decrease in the amount of protein on SDS-PAGE gels for glucose incubated SOD and formation of high molecular weight aggregates for MG or both glucose and MG incubated enzyme. Glucose 188-195 superoxide dismutase 1 Homo sapiens 206-209 24412154-6 2014 Incubation of SOD with glucose, MG or both at 37 C resulted in a progressive decrease in the activity of the enzyme, and a parallel decrease in the amount of protein on SDS-PAGE gels for glucose incubated SOD and formation of high molecular weight aggregates for MG or both glucose and MG incubated enzyme. Glucose 188-195 superoxide dismutase 1 Homo sapiens 14-17 24412154-6 2014 Incubation of SOD with glucose, MG or both at 37 C resulted in a progressive decrease in the activity of the enzyme, and a parallel decrease in the amount of protein on SDS-PAGE gels for glucose incubated SOD and formation of high molecular weight aggregates for MG or both glucose and MG incubated enzyme. Glucose 188-195 superoxide dismutase 1 Homo sapiens 206-209 24412154-7 2014 TQ offered protection against glucose or MG induced loss in SOD activity and fragmentation/cross-linking. Glucose 30-37 superoxide dismutase 1 Homo sapiens 60-63 24420848-7 2014 After 12 h-incubation, MET significantly inhibited the increase of MDA, TNF-alpha, LDH and CK levels induced by high glucose, especially at the 5 x 10(-5) to 10(-4 )mol/L concentrations while inhibiting the decrease of SOD level. Glucose 117-124 superoxide dismutase 1 Homo sapiens 219-222 24933520-4 2014 Incubation of SOD with glucose, methylglyoxal (MG) or both at 37C resulted in progressive hyperchromicity at 280nm, intrinsic fluorescence quenching at 310nm, decrease in negative ellipticity at 208nm, AGE-specific fluorescence enhancement in the wavelength range 400-480nm and Thioflavin T (ThT) fluorescence enhancement at 480nm (fibrillar state enhancement). Glucose 23-30 superoxide dismutase 1 Homo sapiens 14-17 24933520-5 2014 Therefore, glycation by glucose or MG induced both tertiary and secondary structural changes in SOD and formation of AGEs and fibrils. Glucose 24-31 superoxide dismutase 1 Homo sapiens 96-99 24933520-7 2014 TQ offered protection against glucose or MG-induced glycation of SOD as observed by a reduction in the structural changes, formation of AGEs and fibrils. Glucose 30-37 superoxide dismutase 1 Homo sapiens 65-68 24439480-6 2014 Switching the energy source from glucose to galactose caused uncoupling of mitochondria with increased proton leak in SOD1(I113T) fibroblasts. Glucose 33-40 superoxide dismutase 1 Homo sapiens 118-122 24439480-7 2014 Assessment of the contribution of fatty acid oxidation to total respiration, suggested that fatty acid oxidation is reduced in SOD1 ALS fibroblasts, an effect which can be mimicked by starving the control cells of glucose. Glucose 214-221 superoxide dismutase 1 Homo sapiens 127-131 24093550-16 2013 In addition, ROS neutralizing enzymes SOD1, GPX1, TXNRD1 and TXNRD2 gene expression were significantly upregulated in high glucose treated HMVEC. Glucose 123-130 superoxide dismutase 1 Homo sapiens 38-42 23332757-6 2013 Therefore, in a single circuit, oxygen, glucose, and reactive oxygen can repress respiration through SOD1/CK1gamma signaling. Glucose 40-47 superoxide dismutase 1 Homo sapiens 101-105 22365984-2 2012 So, the aim of the present study was to investigate the effect of superoxide dismutase (SOD) like activity protein, partially purified from radish (Rhaphnus sativa) on uptake of glucose in vitro by erythrocytes of diabetic patients. Glucose 178-185 superoxide dismutase 1 Homo sapiens 88-91 23026387-7 2012 The addition of exogenous CAT and SOD significantly protected the capacity for glucose uptake and respiration, suggesting that superoxide and H(2)O(2) are involved in the impairment of activity during UV-B exposure. Glucose 79-86 superoxide dismutase 1 Homo sapiens 34-37 23691521-5 2013 Glucose loading lowered flow-mediated endothelium-dependent dilation (FMEDD), NO, and superoxide dismutase (SOD) (P < 0.01). Glucose 0-7 superoxide dismutase 1 Homo sapiens 86-106 23691521-5 2013 Glucose loading lowered flow-mediated endothelium-dependent dilation (FMEDD), NO, and superoxide dismutase (SOD) (P < 0.01). Glucose 0-7 superoxide dismutase 1 Homo sapiens 108-111 22365984-5 2012 The glucose uptake by erythrocytes of diabetic patients was highly significantly decreased (P < 0.0001) with increasing hyperglycemia, while it was highly significantly elevated (p < 0.0001) after addition of the partially purified SOD like activity protein. Glucose 4-11 superoxide dismutase 1 Homo sapiens 238-241 22365984-7 2012 It thus can be concluded that, an appropriate support for enhancing antioxidant supply, such as SOD like activity protein from natural sources, may help control blood glucose level and may prevent clinical complications of diabetes. Glucose 167-174 superoxide dismutase 1 Homo sapiens 96-99 21656919-7 2011 The major effect of the expression of SOD on the activity of the TFs was observed in the early stationary phase with 34 of them perturbed in comparison with 12 on glucose and 20 on ethanol. Glucose 163-170 superoxide dismutase 1 Homo sapiens 38-41 21530659-9 2011 These findings suggest that the glutathione decrease associated with mutant SOD1 expression is due to mitochondrial dysfunction caused by the reduction of the flow of glucose-derived pyruvate through the TCA cycle; it implies altered glutamate metabolism and depends on the different mitochondrial energy substrates. Glucose 167-174 superoxide dismutase 1 Homo sapiens 76-80 22425406-5 2012 RESULTS: SOD1 treatment diminished high glucose-induced oxidative stress, as evidenced by 4-hydroxynonenal and malondialdehyde reductions, and it blocked high glucose-increased iNOS expression, iNOS-luciferase activities, and nitrosylated protein. Glucose 40-47 superoxide dismutase 1 Homo sapiens 9-13 22425406-5 2012 RESULTS: SOD1 treatment diminished high glucose-induced oxidative stress, as evidenced by 4-hydroxynonenal and malondialdehyde reductions, and it blocked high glucose-increased iNOS expression, iNOS-luciferase activities, and nitrosylated protein. Glucose 159-166 superoxide dismutase 1 Homo sapiens 9-13 22073946-4 2011 RESULTS: The activity of SOD1 was the lowest in GLCs treated with 100 microM DDC as compared to control cells and to the cells supplemented with Cu, Zn-SOD or DDC (10 microM). Glucose 48-52 superoxide dismutase 1 Homo sapiens 25-29 19362569-9 2009 Administration of superoxide dismutase (SOD) decreased O(2)(-) concentration and increased NO concentration, thus SOD improved high glucose-induced changes in these interactions. Glucose 132-139 superoxide dismutase 1 Homo sapiens 18-38 21237524-5 2011 RESULTS: With the abnormality of glucose and lipid metabolism, diabetic patients showed a higher oxidative stress state indicated by decreased SOD activity but elevated MDA and protein carbonylation level. Glucose 33-40 superoxide dismutase 1 Homo sapiens 143-146 19819039-3 2009 Serum SOD activity negatively correlated with body mass index (BMI), systolic and diastolic blood pressure, serum triglyceride (TG) concentration and serum glucose concentration. Glucose 156-163 superoxide dismutase 1 Homo sapiens 6-9 19878539-10 2009 SOD treatment of glucose-stressed EPCs attenuated O2- generation, restored NO production, and partially restored their ability to form colonies. Glucose 17-24 superoxide dismutase 1 Homo sapiens 0-3 19362569-9 2009 Administration of superoxide dismutase (SOD) decreased O(2)(-) concentration and increased NO concentration, thus SOD improved high glucose-induced changes in these interactions. Glucose 132-139 superoxide dismutase 1 Homo sapiens 40-43 19362569-9 2009 Administration of superoxide dismutase (SOD) decreased O(2)(-) concentration and increased NO concentration, thus SOD improved high glucose-induced changes in these interactions. Glucose 132-139 superoxide dismutase 1 Homo sapiens 114-117 18937644-6 2009 Overexpression of manganese SOD (superoxide dismutase) and mitochondrially targeted catalase significantly protected HCT116 and MB231 cells from glucose-deprivation-induced cytotoxicity and oxidative stress and also protected HT29 cells from 2DG-induced cytotoxicity. Glucose 145-152 superoxide dismutase 1 Homo sapiens 28-31 18937644-6 2009 Overexpression of manganese SOD (superoxide dismutase) and mitochondrially targeted catalase significantly protected HCT116 and MB231 cells from glucose-deprivation-induced cytotoxicity and oxidative stress and also protected HT29 cells from 2DG-induced cytotoxicity. Glucose 145-152 superoxide dismutase 1 Homo sapiens 33-53 17880913-11 2008 CONCLUSION: The results suggest that gingival-SOD activity increases in diabetes and decreases in periodontitis and relations may exist between gingival-SOD activity, periodontal status, HbA1c, glucose and HDL levels. Glucose 194-201 superoxide dismutase 1 Homo sapiens 46-49 18215717-7 2008 HO-1 protein expression in HUVECs exposed to 20 mM of glucose was increased in the presence of 20 U/ml superoxide dismutase (SOD). Glucose 54-61 superoxide dismutase 1 Homo sapiens 103-123 18215717-7 2008 HO-1 protein expression in HUVECs exposed to 20 mM of glucose was increased in the presence of 20 U/ml superoxide dismutase (SOD). Glucose 54-61 superoxide dismutase 1 Homo sapiens 125-128 15936462-5 2005 CD, TBARS and SOD values were positively correlated with plasma glucose concentration and glycated hemoglobin level. Glucose 64-71 superoxide dismutase 1 Homo sapiens 14-17 15983321-7 2005 At high glucose concentrations, the activity and mRNA expression of CuZnSOD increased similarly in all groups (diabetic subjects with angiopathy: 0.93 +/- 0.26 units/mg protein, 9.4 +/- 2.1 mRNA); that of CAT and GPX increased in only control subjects and diabetic subjects without angiopathy (diabetic subjects with angiopathy: 0.33 +/- 0.09 units/mg protein and 5.0 +/- 1.4 mRNA; 0.54 +/- 0.10 units/mg protein and 2.3 +/- 1.0 mRNA, respectively). Glucose 8-15 superoxide dismutase 1 Homo sapiens 68-75 15983321-6 2005 RESULTS: At a normal glucose concentration (5 mmol/l), the activity and mRNA expression of CuZnSOD (0.50 +/- 0.21 units/mg protein, 4.4 +/- 1.5 mRNA/glyceraldehyde-3-phosphate dehydrogenase), MnSOD (0.26 +/- 0.04 units/mg protein, 0.08 +/- 0.07 mRNA), CAT (0.32 +/- 0.08 units/mg protein, 4.8 +/- 1.3 mRNA), and GPX (0.53 +/- 0.09 units/mg protein, 2.2 +/- 0.9 mRNA) were not different among the three groups (only values of diabetic subjects with angiopathy are shown). Glucose 21-28 superoxide dismutase 1 Homo sapiens 91-98 11555836-6 2001 In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad. Glucose 60-67 superoxide dismutase 1 Homo sapiens 23-26 12811469-6 2003 RESULTS: Interaction of EC with SMC pre-exposed to high glucose concentration yielded changes in endothelial Ca(2+) signalling and polymerization of f-actin in a concentration-dependent and superoxide dismutase (SOD) sensitive manner. Glucose 56-63 superoxide dismutase 1 Homo sapiens 190-210 12811469-6 2003 RESULTS: Interaction of EC with SMC pre-exposed to high glucose concentration yielded changes in endothelial Ca(2+) signalling and polymerization of f-actin in a concentration-dependent and superoxide dismutase (SOD) sensitive manner. Glucose 56-63 superoxide dismutase 1 Homo sapiens 212-215 12626432-7 2003 The mutated Cu, Zn-SOD incubated with glucose generated higher levels of hydrogen peroxide than the wild-type enzyme. Glucose 38-45 superoxide dismutase 1 Homo sapiens 19-22 11522679-7 2001 In vitro infection of mesangial cells (MC) with a recombinant adenovirus encoding human SOD-1 increased SOD-1 activity threefold over control cells and prevented the reduction of aconitase activity, an index of cellular superoxide, and the increase in collagen synthesis that otherwise occurred in control MC in response to culture with 300 or 500 mg/dl glucose. Glucose 354-361 superoxide dismutase 1 Homo sapiens 88-93 15784031-6 2005 CuZn-superoxide dismutase levels were negatively associated with glucose, insulin, and HOMA-IR. Glucose 65-72 superoxide dismutase 1 Homo sapiens 0-25 15493452-17 2004 However, after mean glucose levels in the studied group were included into these analyses, this relationship was only evident with SOD and GPX activity (p < 0.0016). Glucose 20-27 superoxide dismutase 1 Homo sapiens 131-134 12898015-6 2003 The high glucose-induced abnormalities were abrogated or attenuated by urate, MnTBAP, L-NMMA, BH(4), and SOD, whereas unaffected by haemoglobin, PTIO and NH(4). Glucose 9-16 superoxide dismutase 1 Homo sapiens 105-108 14605996-7 2003 Cu-Zn SOD activities were significantly increased in subjects with NGT, and were significantly decreased in subjects with IGT and DGT (p< 0.001 and p< 0.001) after glucose loading. Glucose 170-177 superoxide dismutase 1 Homo sapiens 0-9 12584757-1 2003 The synthesis of human superoxide dismutase (SOD) in batch cultures of a Saccharomyces cerevisiae strain using a glucose-limited minimal medium was studied through metabolic flux analysis. Glucose 113-120 superoxide dismutase 1 Homo sapiens 23-43 12584757-1 2003 The synthesis of human superoxide dismutase (SOD) in batch cultures of a Saccharomyces cerevisiae strain using a glucose-limited minimal medium was studied through metabolic flux analysis. Glucose 113-120 superoxide dismutase 1 Homo sapiens 45-48 12584757-5 2003 The synthesis of SOD by the strain P+ resulted in a decrease in specific growth rate of 34 and 54% (growth on glucose and ethanol respectively) in comparison to the wild type. Glucose 110-117 superoxide dismutase 1 Homo sapiens 17-20 12621526-8 2003 D-Glucose-dependent inhibition of thymidine incorporation and cell proliferation is associated with increased PKC, eNOS, and MEK1/2, but decreased SOD activity, and higher intracellular levels of cGMP, cAMP and Ca2+ in HUVECs. Glucose 0-9 superoxide dismutase 1 Homo sapiens 147-150 14610325-8 2003 The inhibitory effect of high glucose on NO production was restored by the addition of SOD. Glucose 30-37 superoxide dismutase 1 Homo sapiens 87-90 11555836-6 2001 In cells infected with SOD-2 (SOD-2-Ad) and cultured in low glucose, SOD-2 activity was 5-fold higher than in cells infected with GFP (GFP-Ad), whereas Cu(2+)/Zn(2+) cytoplasmic SOD (SOD-1) did not differ; culture in high-glucose media did not alter SOD-2 or SOD-1 activity in either GFD-Ad or SOD-2-Ad. Glucose 222-229 superoxide dismutase 1 Homo sapiens 23-26 10984191-9 2000 The cells expressing hSOD1 showed enhanced survival in glucose- and pyruvate-free medium. Glucose 55-62 superoxide dismutase 1 Homo sapiens 21-26 11118022-5 2000 Under high-glucose conditions, CuZnSuperoxide-dismutase mRNA and activity increased similarly in all groups (P < 0.001 vs. basal), whereas MnSuperoxide-dismutase did not change. Glucose 11-18 superoxide dismutase 1 Homo sapiens 31-55 7998936-13 1994 Incubation of isolated nuclei with Cu,Zn-SOD that had been pre-incubated with glucose also resulted in nuclear DNA cleavage. Glucose 78-85 superoxide dismutase 1 Homo sapiens 35-44 10984077-10 2000 Hyperglycemia increased plasma MDA concentrations, but the activities of GSH-Px and SOD were significantly higher after a larger dose of glucose only. Glucose 137-144 superoxide dismutase 1 Homo sapiens 84-87 9794110-4 1998 There was evidence of oxidative stress as indicated by a 50% increase in intracellular malondialdehyde (p < 0.05), increased mRNA expression of CuZn superoxide dismutase and Mn superoxide dismutase (by 51% and 37% respectively, p < 0.01) and a 50% decrease in glutathione in 25 mmol/l D-glucose (p < 0.001). Glucose 291-300 superoxide dismutase 1 Homo sapiens 147-172 9438984-2 1997 The change of the activity and the molecular weight were measured and compared with that of SOD incubated with glucose or fructose. Glucose 111-118 superoxide dismutase 1 Homo sapiens 92-95 8150417-5 1994 All these results were consistent with the in vivo studies that Cu,Zn-superoxide dismutase activity in erythrocytes of non-insulin dependent diabetic patients was inversely correlated with their plasma glucose. Glucose 202-209 superoxide dismutase 1 Homo sapiens 64-90 35129966-6 2022 The PEG-DA/HA-PBA/MY (PHM) hybrid hydrogel achieved glucose-triggered MY release, efficient ROS-scavenging (>80.0%), and also reshaped the hostile oxidative wound microenvironment (reduced MDA activity and increased SOD and GSH/GSSG levels). Glucose 52-59 superoxide dismutase 1 Homo sapiens 216-219 1326527-9 1992 Incubation with glucose resulted in a time-dependent release of Cu2+ from the Cu,Zn-SOD molecule. Glucose 16-23 superoxide dismutase 1 Homo sapiens 78-87 34282379-10 2021 The activity of CAT and SOD showed a decrease and the content of ROS and the ratio of GSSG/T-GSH showed an increase in high glucose and AGEs-BSA group. Glucose 124-131 superoxide dismutase 1 Homo sapiens 24-27 34284711-4 2021 2-Deoxyglucose, an inhibitor of glycolysis, and propyl gallate, SOD-mimic and antioxidant, suppressed destruction of the nuclei that was caused by SOD inhibitors and glucose in cells of the epidermis from the young, but not from the old leaves. Glucose 166-173 superoxide dismutase 1 Homo sapiens 64-67 35401165-5 2022 The in vitro results showed that: 1) Fr increased the expression of antioxidant enzymes including SOD1 and HO-1 to inhibit high glucose (HG)-induced fibronectin (FN) and inflammatory cell adhesion molecule (ICAM-1) overexpression; 2) Fr exerted antioxidant effect through activating the Nrf2/ARE pathway; 3) Fr significantly up-regulated the expression of Cx43 in HG-induced glomerular mesangial cells (GMCs), while the knock down of Cx43 largely impaired the activation of Nrf2/ARE pathway induced by Fr; 4) Fr promoted the activation of Nrf2/ARE pathway via regulating the interaction between Cx43 and AKT. Glucose 128-135 superoxide dismutase 1 Homo sapiens 98-102 3567220-3 1987 The nonglucosylated form of Cu-Zn-superoxide dismutase, which was washed through the boronate column, was glucosylated in vitro upon exposure to radioactive or non-radioactive D-glucose. Glucose 176-185 superoxide dismutase 1 Homo sapiens 28-54 3248772-3 1988 The nonglycosylated Cu-Zn-superoxide dismutase, which was washed through the boronate column, was glycosylated in vitro upon exposure to radioactive or nonradioactive D-glucose. Glucose 167-176 superoxide dismutase 1 Homo sapiens 20-46 33913390-7 2021 The linear correlation (all at p < 0.05) showed correlation for Res&triacylglycerols (R = 0.44), and for Res&diastolic blood pressure (R = -0.58) and for SOD-1&fasting glucose (R = -0.34) in MetS, while in the non-MetS group fasting glucose correlates with Res (R = 0.58) and with TAS (R = -0.43). Glucose 168-175 superoxide dismutase 1 Homo sapiens 154-159 32643032-7 2021 Then, we measured the generation of ROS, the activities of total superoxide dismutase (SOD), and total antioxidant capacity (TAC) of the cells; the results showed that high glucose destroyed cells by inducing high concentration of ROS, the balance of oxidation, and antioxidation cause oxidative stress damage to cells. Glucose 173-180 superoxide dismutase 1 Homo sapiens 65-85 32643032-7 2021 Then, we measured the generation of ROS, the activities of total superoxide dismutase (SOD), and total antioxidant capacity (TAC) of the cells; the results showed that high glucose destroyed cells by inducing high concentration of ROS, the balance of oxidation, and antioxidation cause oxidative stress damage to cells. Glucose 173-180 superoxide dismutase 1 Homo sapiens 87-90 6213639-6 1982 When islets were protected from alloxan toxicity by including 28 mM glucose with alloxan, the insulin secretory response and SOD specific activity remained identical to controls. Glucose 68-75 superoxide dismutase 1 Homo sapiens 125-128 33913390-7 2021 The linear correlation (all at p < 0.05) showed correlation for Res&triacylglycerols (R = 0.44), and for Res&diastolic blood pressure (R = -0.58) and for SOD-1&fasting glucose (R = -0.34) in MetS, while in the non-MetS group fasting glucose correlates with Res (R = 0.58) and with TAS (R = -0.43). Glucose 233-240 superoxide dismutase 1 Homo sapiens 154-159 32617139-9 2020 SOD activity is modestly correlated with glucose indicators and insulin sensitivity and beta-cell function indices and was independently and negatively correlated with the level of triglyceride. Glucose 41-48 superoxide dismutase 1 Homo sapiens 0-3 33655586-11 2021 In addition, MDA, LDH, and SOD were increased after high glucose induction, while decreased after AZM treatment (p < .001). Glucose 57-64 superoxide dismutase 1 Homo sapiens 27-30 33229451-1 2020 OBJECTIVE: To identify the metabolic changes related to the various levels of cognitive deficits in amyotrophic lateral sclerosis (ALS) using 18F-2-fluoro-2-deoxy-D-glucose positron emission tomography (18F-FDG-PET) imaging. Glucose 165-172 superoxide dismutase 1 Homo sapiens 131-134 32908567-10 2020 In the partially controlled blood glucose, increment of SOD activity in the CAo + CAt group was greater than that in the control group (p = 0.01). Glucose 34-41 superoxide dismutase 1 Homo sapiens 56-59 32908567-11 2020 There were medium-to-strong correlation between CML with SOD (r = 0.58, p < 0.05) and IL-1alpha with SOD (r = 0.70, p < 0.05) in well-controlled blood glucose. Glucose 151-158 superoxide dismutase 1 Homo sapiens 101-104 32908567-13 2020 Conclusion: CAo and CAt combination can be used to significantly improve dry skin condition through increasing SOD activity in T2DM patients with controlled blood glucose. Glucose 163-170 superoxide dismutase 1 Homo sapiens 111-114 32339204-8 2020 RESULTS: High glucose caused HLE cells oxidative stress and apoptosis exhibiting the increase of apoptotic cells and ROS production and decrease of bcl-2/bax ratio, GSH/GSSG ration and SOD activity. Glucose 14-21 superoxide dismutase 1 Homo sapiens 185-188 32018221-5 2020 In addition, high-glucose (50 mM) significantly decreased the levels of miR-130a and superoxide dismutase (SOD) 1, and promoted tumor necrosis factor (TNF)-alpha expressions in ARPE-19 cells. Glucose 18-25 superoxide dismutase 1 Homo sapiens 85-113 32018221-7 2020 Furthermore, overexpression of miR-130a abrogated the effects of high-glucose (50 mM) on the above cell functions, which were all reversed by either upregulating TNF-alpha or knocking down SOD1 in ARPE-19 cells. Glucose 70-77 superoxide dismutase 1 Homo sapiens 189-193 32018221-8 2020 Taken together, upregulation of miR-130a alleviated the cytotoxic effects of high-glucose (50 mM) on ARPE-19 cells by regulating TNF-alpha/SOD1/ROS axis mediated pyroptotic cell death. Glucose 82-89 superoxide dismutase 1 Homo sapiens 139-143 32018221-0 2020 MiR-130a alleviated high-glucose induced retinal pigment epithelium (RPE) death by modulating TNF-alpha/SOD1/ROS cascade mediated pyroptosis. Glucose 25-32 superoxide dismutase 1 Homo sapiens 104-108 32271403-13 2020 Besides, high glucose promoted the expression of 8-OH, and inhibited SOD1, SOD2, and CAT mRNA expressions, resulting in the up-regulated ROS level of CHs. Glucose 14-21 superoxide dismutase 1 Homo sapiens 69-73 30466006-6 2019 EA upregulated glucose consumption, IRS1, Akt and ERK phosphorylation under insulin stimulation, reduced ROS and O2- production and MDA level, and increased SOD activity in high glucose-exposed HepG2 cells. Glucose 178-185 superoxide dismutase 1 Homo sapiens 157-160 30142540-11 2018 RESULTS: High glucose induced the increase of ROS level, activation of TXNIP, but restricted mitochondrial membrane potential and activities of p-AMPK, SOD and CAT, and Trx. Glucose 14-21 superoxide dismutase 1 Homo sapiens 152-155 30092096-11 2018 The mRNA levels of heme oxygenase-1 and superoxide dismutase-1 and ROS levels were significantly increased in HGFs after 72 h of exposure to 50 mM glucose concentration. Glucose 147-154 superoxide dismutase 1 Homo sapiens 40-62