title: Oxidative stress after subarachnoid hemorrhage in gp91phox knockout mice.
abstract: BACKGROUND
  Oxidative stress largely contributes to early brain injury after subarachnoid hemorrhage (SAH). One of the major sources of reactive oxygen species is NADPH oxidase, upregulated after SAH. We hypothesized that NADPH oxidase-induced oxidative stress plays a major causative role in early brain injury after SAH.
  
  
  METHODS
  Using gp91phox knockout (ko) and wild-type (wt) mice, we studied early brain injury in the endovascular perforation model of SAH. Mortality rate, cerebral edema, oxidative stress, and superoxide production were measured at 24 h after SAH. Neurological evaluation was done at 23 h after SAH surgery.
  
  
  RESULTS
  Genotyping confirmed the existence of a nonfunctional gp91phox gene in the ko mice. CBF measurements did not show differences in SAH-induced acute ischemia between ko and wt mice. SAH caused a significant increase of water content in the ipsilateral hemisphere as well as an increase of Malondialdehyde (MDA) levels and superoxide production. There were no significant differences in post-SAH mortality rate, brain water content and the intensity of the oxidative stress between knockout and wild type groups of mice.
  
  
  CONCLUSIONS
  Our results suggest that gp91phox is not critically important to the early brain injury after SAH. An adaptive compensatory mechanism for free radical production in knockout mice is discussed.
authors.affiliation: Department of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, USA.
authors.forename: Shimin
authors.initials: S
authors.lastname: Liu
authors.forename: Jiping
authors.initials: J
authors.lastname: Tang
authors.forename: Robert P
authors.initials: RP
authors.lastname: Ostrowski
authors.forename: Elena
authors.initials: E
authors.lastname: Titova
authors.forename: Cara
authors.initials: C
authors.lastname: Monroe
authors.forename: Wanqiu
authors.initials: W
authors.lastname: Chen
authors.forename: Wendy
authors.initials: W
authors.lastname: Lo
authors.forename: Robert
authors.initials: R
authors.lastname: Martin
authors.forename: John H
authors.initials: JH
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000201:enzymology / Q000503:physiopathology; D001925:Brain Damage, Chronic / Q000201:enzymology / Q000235:genetics* / Q000503:physiopathology; D001929:Brain Edema / Q000201:enzymology / Q000235:genetics / Q000503:physiopathology; D002536:Cerebral Arteries / Q000201:enzymology / Q000503:physiopathology; D005609:Free Radicals / Q000378:metabolism; D005819:Genetic Markers / Q000235:genetics; D008297:Male; D008562:Membrane Glycoproteins / Q000235:genetics*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D000074662:NADPH Oxidase 2; D019255:NADPH Oxidases / Q000235:genetics*; D009410:Nerve Degeneration / Q000201:enzymology / Q000235:genetics* / Q000503:physiopathology; D018384:Oxidative Stress / Q000235:genetics*; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000201:enzymology / Q000503:physiopathology; D013481:Superoxides / Q000378:metabolism