PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
15686499-6	2005	It is concluded that L-type Ca2+ channels are a primary target of SIN-1-induced extracellular nitrosative/oxidative stress, being inactivated by chronic exposure to fluxes of peroxynitrite of 0.5-1 microm/min, while higher concentrations of peroxynitrite and hydrogen peroxide are required for the inhibition of the plasma membrane Ca2+ ATPase and induction of necrotic cell death, respectively.	Hydrogen Peroxide	259-276	MAPK associated protein 1	Homo sapiens	66-71	
12466224-7	2002	Hydroxycobalamin, a NO scavenger, but not superoxide dismutase and catalase, enzymes that metabolize superoxide and hydrogen peroxide, respectively, abolished the inhibitory effect of DEA/NO and SIN-1, indicating that they inhibit DA uptake through a mechanism related to the production of NO but unrelated to the formation of peroxynitrite.	Hydrogen Peroxide	116-133	MAPK associated protein 1	Homo sapiens	195-200	
15622856-5	2004	NADH was found to be less sensitive than dihydrorhodamine 123 and 2",7"-dichlorodihydrofluorescein diacetate to oxidation by H2O2, which is produced during SIN-1 decomposition in common buffers.	Hydrogen Peroxide	125-129	MAPK associated protein 1	Homo sapiens	156-161	
10471084-2	1999	In this context, we have previously shown that cyclic GMP elevations confer cytoprotection against the neurotoxicity induced by SIN-1 in the presence of superoxide dismutase, conditions in which cell death seems to be a consequence of hydrogen peroxide (H2O2) formation.	Hydrogen Peroxide	235-252	MAPK associated protein 1	Homo sapiens	128-133	
12417336-4	2002	In addition, we show that, in contrast to the reversible inhibition of NSM1 by H2O2 or GSSG which involves the formation of disulfide bonds, irreversible inactivation of this enzyme by peroxynitrite generated from SIN1 is likely due to definitive oxidative thiol modification.	Hydrogen Peroxide	79-83	MAPK associated protein 1	Homo sapiens	214-218	
11677273-9	2001	and the subsequently formed H(2)O(2) by superoxide dismutase (SOD) plus catalase likewise prevented the nitration of protein-bound tyrosine but actually enhanced the cytotoxicity of SIN-1, indicating that cortical cells can cope with the oxidative but not the nitrosative stress generated.	Hydrogen Peroxide	28-36	MAPK associated protein 1	Homo sapiens	182-187	
10471084-2	1999	In this context, we have previously shown that cyclic GMP elevations confer cytoprotection against the neurotoxicity induced by SIN-1 in the presence of superoxide dismutase, conditions in which cell death seems to be a consequence of hydrogen peroxide (H2O2) formation.	Hydrogen Peroxide	254-258	MAPK associated protein 1	Homo sapiens	128-133	
9202724-3	1997	In the present study, we have compared SIN-1, which generates nitric oxide, superoxide anion and hydrogen peroxide, with two other nitric oxide donors, S-nitrosoglutathione (GSNO) and the tetra-iron-sulphur cluster nitrosyl, Roussin"s black salt (RBS).	Hydrogen Peroxide	97-114	MAPK associated protein 1	Homo sapiens	39-44	
9582295-4	1998	Whereas in mere phosphate buffer H2O2 formation from 1.5 mM SIN-1 was low ( approximately 15 microM), incubation of SIN-1 with Good"s buffer compounds resulted in continuous H2O2 formation.	Hydrogen Peroxide	174-178	MAPK associated protein 1	Homo sapiens	116-121	
9582295-5	1998	After 2 h of incubation of 1.5 mM SIN-1 with 20 mM HEPES about 190 microM H2O2 were formed.	Hydrogen Peroxide	74-78	MAPK associated protein 1	Homo sapiens	34-39	
9582295-6	1998	The same amount of H2O2 could be achieved from 1.5 mM SIN-1 by action of superoxide dismutase in the absence of HEPES.	Hydrogen Peroxide	19-23	MAPK associated protein 1	Homo sapiens	54-59	
9582295-9	1998	Furthermore, the peroxynitrite scavenger tryptophan significantly reduced H2O2 formation from SIN-1-HEPES interactions.	Hydrogen Peroxide	74-78	MAPK associated protein 1	Homo sapiens	94-99	
9441903-2	1997	A 6-h preincubation with linsidomine (SIN-1, 0.5 mM) protected endothelial cells from hydrogen peroxide-dependent cytotoxicity and increased the surviving endothelial cell fraction by 85%.	Hydrogen Peroxide	86-103	MAPK associated protein 1	Homo sapiens	38-43	
9202724-12	1997	In addition, H2O2 may be formed in the presence of SIN-1 and may form hydroxyl radical in the presence of a transition metal, such as Fe2+.	Hydrogen Peroxide	13-17	MAPK associated protein 1	Homo sapiens	51-56	
8769740-7	1996	Cells previously exposed to SNAP and SIN-1 exhibited a significant protection against the cytotoxicity mediated by hydrogen peroxide (250 microM) (P < 0.05).	Hydrogen Peroxide	115-132	MAPK associated protein 1	Homo sapiens	37-42	
8660704-7	1996	3-Morpholinosynodiomine.HCl (SIN-1) and sodium nitroprusside (SNP) enhanced hydrogen peroxide-mediated cytotoxicity, while S-nitrosoglutathione (GSNO), and S-nitroso-N-acetylpenicillamine (SNAP) afforded protection.	Hydrogen Peroxide	76-93	MAPK associated protein 1	Homo sapiens	29-34	
23567270-6	2013	Purified, recombinant PGIS showed a half-maximal nitration by 10 muM 3-morpholino sydnonimine (Sin-1) which increased in the presence of bicarbonate, and was only marginally induced by freely diffusing NO2-radicals generated by a peroxidase/nitrite/hydrogen peroxide system.	Hydrogen Peroxide	249-266	MAPK associated protein 1	Homo sapiens	95-100	
24639107-8	2014	We found that exposure to exogenous H2O2 or incubation of dispersed gastric muscle cells with SIN-1 significantly increased the expression of calponin, caldesmon, and smoothelin proteins.	Hydrogen Peroxide	36-40	MAPK associated protein 1	Homo sapiens	94-99	
7673115-11	1995	In the presence of SIN-1, Mn-SOD increased accumulation of H2O2 in a concentration-dependent manner.	Hydrogen Peroxide	59-63	MAPK associated protein 1	Homo sapiens	19-24	
7673115-12	1995	In contrast, Cu,Zn-SOD increased H2O2 accumulation from SIN-1 at low but not high concentrations of the enzyme, suggesting that high concentrations of the Cu,Zn-SOD interacted with the H2O2.	Hydrogen Peroxide	33-37	MAPK associated protein 1	Homo sapiens	56-61	
7673115-12	1995	In contrast, Cu,Zn-SOD increased H2O2 accumulation from SIN-1 at low but not high concentrations of the enzyme, suggesting that high concentrations of the Cu,Zn-SOD interacted with the H2O2.	Hydrogen Peroxide	185-189	MAPK associated protein 1	Homo sapiens	56-61	
21497204-8	2011	SIN-1 decomposition products, NO and superoxide anion or peroxynitrite, induced greater cytotoxicity in lymphocyte cultures (separately and in whole blood) supplemented with HEPES - the organic buffer that is widely used to maintain stable physiological pH in cell cultures -, due to H(2)O(2) production, than in cultures without HEPES.	Hydrogen Peroxide	284-292	MAPK associated protein 1	Homo sapiens	0-5	
18841468-3	2009	We demonstrated in vitro that the amount of ONOO(-) generated and H(2)O(2) formation directly correlated with SIN-1 concentration.	Hydrogen Peroxide	66-74	MAPK associated protein 1	Homo sapiens	110-115