title: NAD(P)H oxidase, superoxide dismutase, catalase, glutathione peroxidase and nitric oxide synthase expression in subacute spinal cord injury.
abstract: Primary trauma to the spinal cord triggers a cascade of cellular and molecular events that promote continued tissue damage and expansion of the lesion for extended periods following the initial injury. Oxidative and nitrosative stresses play an important role in progression of spinal cord injury (SCI). In an attempt to explore the biochemical origin of oxidative/nitrosative stress associated with secondary SCI, we studied expression of the superoxide (O2*-)-generating enzyme, NAD(P)H oxidase, antioxidant enzymes [superoxide dismutase (CuZn SOD, Mn SOD), catalase, glutathione peroxidase (GPX)], nitric oxide synthases (NOS) and a byproduct of NO-O2*- interaction (nitrotyrosine) in the spinal cord tissues of rats 16 h and 14 days after surgical resections of a 5-mm segment of the cord below T8 or sham-operation. Immunodetectable NAD(P)H oxidase subunits (gp91phox and P67phox), Mn SOD, inducible NOS (iNOS), endothelial NOS (eNOS), and nitrotyrosine were elevated in the transected cords on day 1 and day 14. Neuronal NOS (nNOS) was unchanged on day 1 and significantly depressed on day 14. GPX was unchanged on day 1 and significantly elevated on day 14. Catalase was unchanged in the cord tissue surrounding the transection site at both points. Thus, concurrent upregulations of NAD(P)H oxidase, eNOS and iNOS (but not nNOS), work in concert to maintain oxidative and nitrosative stress in the injured cord tissue.
authors.affiliation: Division of Nephrology and Hypertension, University of California at Irvine Medical Center, 101 The City Drive, Building 53, Room 125, Rt. 81, Orange, CA 92868, USA. ndvaziri@uci.edu
authors.forename: Nosratola D
authors.initials: ND
authors.lastname: Vaziri
authors.forename: Yu-Shang
authors.initials: YS
authors.lastname: Lee
authors.forename: Ching-Yi
authors.initials: CY
authors.lastname: Lin
authors.forename: Vernon W
authors.initials: VW
authors.lastname: Lin
authors.forename: Ram K
authors.initials: RK
authors.lastname: Sindhu
mesh_terms: D000208:Acute Disease; D000818:Animals; D002374:Catalase / Q000378:metabolism*; D005260:Female; D016166:Free Radical Scavengers / Q000378:metabolism; D020233:Gait Disorders, Neurologic / Q000201:enzymology / Q000209:etiology / Q000503:physiopathology; D005979:Glutathione Peroxidase / Q000378:metabolism*; D006614:Hindlimb / Q000503:physiopathology; D019255:NADPH Oxidases / Q000378:metabolism*; D009474:Neurons / Q000201:enzymology / Q000473:pathology; D009566:Nitrates / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D015538:Nitrosation; D018384:Oxidative Stress / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D020127:Recovery of Function / Q000502:physiology; D013116:Spinal Cord / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D013482:Superoxide Dismutase / Q000378:metabolism*
chemical_list: D016166:Free Radical Scavengers; D009566:Nitrates; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D002374:Catalase; D005979:Glutathione Peroxidase; D019001:Nitric Oxide Synthase; D013482:Superoxide Dismutase; D019255:NADPH Oxidases