PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
12456489-2	2002	Using genetically altered mice to enhance or disrupt extracellular superoxide dismutase (EC-SOD, SOD3), we tested the hypothesis that this enzyme plays a critical role in the physiological response to oxygen in the brain by regulating nitric oxide (NO*) availability.	Oxygen	201-207	superoxide dismutase 3, extracellular	Mus musculus	53-87	
12456489-2	2002	Using genetically altered mice to enhance or disrupt extracellular superoxide dismutase (EC-SOD, SOD3), we tested the hypothesis that this enzyme plays a critical role in the physiological response to oxygen in the brain by regulating nitric oxide (NO*) availability.	Oxygen	201-207	superoxide dismutase 3, extracellular	Mus musculus	89-95	
12456489-3	2002	Cerebral blood flow responses in these genetically altered mice to changes in PO2 demonstrate that SOD3 regulates equilibrium between superoxide (*O2-) and NO*, thereby controlling vascular tone and reactivity in the brain.	Oxygen	79-81	superoxide dismutase 3, extracellular	Mus musculus	99-103	
12456489-5	2002	Thus, EC-SOD promotes NO* vasodilation by scavenging *O2- while hyperoxia opposes NO* and promotes constriction by enhancing endogenous *O2- generation and decreasing basal vasodilator effects of NO*.	Oxygen	54-56	superoxide dismutase 3, extracellular	Mus musculus	6-12