PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
9740615-0	1998	Role of NADH/NADPH oxidase-derived H2O2 in angiotensin II-induced vascular hypertrophy.	NAD	8-12	angiotensinogen	Homo sapiens	43-57	
9740615-0	1998	Role of NADH/NADPH oxidase-derived H2O2 in angiotensin II-induced vascular hypertrophy.	Hydrogen Peroxide	35-39	angiotensinogen	Homo sapiens	43-57	
9740615-2	1998	We previously showed that angiotensin II (Ang II) increases superoxide production by activating an NADH/NADPH oxidase, which contributes to hypertrophy.	Superoxides	60-70	angiotensinogen	Homo sapiens	26-40	
9740615-2	1998	We previously showed that angiotensin II (Ang II) increases superoxide production by activating an NADH/NADPH oxidase, which contributes to hypertrophy.	Superoxides	60-70	angiotensinogen	Homo sapiens	42-48	
9740615-3	1998	In this study, we determined whether Ang II stimulation of this oxidase results in H2O2 production by studying the effects of Ang II on intracellular H2O2 generation, intracellular superoxide dismutase and catalase activity, and hypertrophy.	Hydrogen Peroxide	83-87	angiotensinogen	Homo sapiens	37-43	
9740615-4	1998	Ang II (100 nmol/L) significantly increased intracellular H2O2 levels at 4 hours.	Hydrogen Peroxide	58-62	angiotensinogen	Homo sapiens	0-6	
9740615-5	1998	Neither superoxide dismutase activity nor catalase activity was affected by Ang II; the SOD present in VSMCs is sufficient to metabolize Ang II-stimulated superoxide to H2O2, which accumulates more rapidly than it is degraded by catalase.	Hydrogen Peroxide	169-173	angiotensinogen	Homo sapiens	76-82	
9740615-5	1998	Neither superoxide dismutase activity nor catalase activity was affected by Ang II; the SOD present in VSMCs is sufficient to metabolize Ang II-stimulated superoxide to H2O2, which accumulates more rapidly than it is degraded by catalase.	Hydrogen Peroxide	169-173	angiotensinogen	Homo sapiens	137-143	
9740615-5	1998	Neither superoxide dismutase activity nor catalase activity was affected by Ang II; the SOD present in VSMCs is sufficient to metabolize Ang II-stimulated superoxide to H2O2, which accumulates more rapidly than it is degraded by catalase.	Hydrogen Peroxide	169-173	catalase	Homo sapiens	229-237	
9740615-6	1998	This increase in H2O2 was inhibited by extracellular catalase, diphenylene iodonium, an inhibitor of the NADH/NADPH oxidase, and the AT1 receptor blocker losartan.	Hydrogen Peroxide	17-21	catalase	Homo sapiens	53-61	
9740615-7	1998	In VSMCs stably transfected with antisense p22phox, a critical component of the NADH/NADPH oxidase in which oxidase activity was markedly reduced, Ang II-induced production of H2O2 was almost completely inhibited, confirming that the source of Ang II-induced H2O2 was the NADH/NADPH oxidase.	Hydrogen Peroxide	176-180	cytochrome b-245 alpha chain	Homo sapiens	43-50	
9740615-7	1998	In VSMCs stably transfected with antisense p22phox, a critical component of the NADH/NADPH oxidase in which oxidase activity was markedly reduced, Ang II-induced production of H2O2 was almost completely inhibited, confirming that the source of Ang II-induced H2O2 was the NADH/NADPH oxidase.	Hydrogen Peroxide	176-180	angiotensinogen	Homo sapiens	147-153	
9740615-7	1998	In VSMCs stably transfected with antisense p22phox, a critical component of the NADH/NADPH oxidase in which oxidase activity was markedly reduced, Ang II-induced production of H2O2 was almost completely inhibited, confirming that the source of Ang II-induced H2O2 was the NADH/NADPH oxidase.	Hydrogen Peroxide	259-263	cytochrome b-245 alpha chain	Homo sapiens	43-50	
9740615-7	1998	In VSMCs stably transfected with antisense p22phox, a critical component of the NADH/NADPH oxidase in which oxidase activity was markedly reduced, Ang II-induced production of H2O2 was almost completely inhibited, confirming that the source of Ang II-induced H2O2 was the NADH/NADPH oxidase.	Hydrogen Peroxide	259-263	angiotensinogen	Homo sapiens	147-153	
9740615-8	1998	Using a novel cell line that stably overexpresses catalase, we showed that this increased H2O2 is a critical step in VSMC hypertrophy, a hallmark of many vascular diseases.	Hydrogen Peroxide	90-94	catalase	Homo sapiens	50-58	
9740615-9	1998	Inhibition of intracellular superoxide dismutase by diethylthiocarbamate (1 mmol/L) also resulted in attenuation of Ang II-induced hypertrophy (62+/-2% inhibition).	Carbamothioic acid, diethyl-	52-72	angiotensinogen	Homo sapiens	116-122