title: Brain antioxidant status in a high pressure-induced rat model of glaucoma.
abstract: OBJECTIVE
  The goal of the present study is to establish the antioxidant status in the brain of a high pressure-induced rat model.
  
  
  METHODS
  Ocular hypertension was induced in rats (n = 12) cauterizing two episcleral veins under a surgical microscope. A sham procedure (n = 12) was performed in the control group. The markers evaluated in the brain 7 days after surgery were as follows: spontaneous chemiluminescence, protein carbonylation, nitrite concentration, total reactive antioxidant potential (TRAP), ascorbic acid, glutathione, vitamin E and activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase.
  
  
  RESULTS
  Chemiluminescence in glaucoma was 55% higher than in controls (393 ± 20 cpm/mg protein, p < 0.001). Protein carbonylation in glaucoma was 93% higher than in controls (1.15 ± 0.18 nmol/mg protein, p < 0.001). Nitrite concentration was 5.30 ± 0.25 μM for glaucoma (controls 4.41 ± 0.24 μM, p < 0.05). Total reactive antioxidant potential decreased by 42% in glaucoma (controls 153 ± 14 μM Trolox, p < 0.001). Ascorbic acid was 67 ± 26 μM for glaucoma (controls 275 ± 22 μM, p < 0.001). Vitamin E was 0.58 ± 0.05 μmol/g organ for glaucoma (controls 1.10 ± 0.06 μmol/g organ, p < 0.01). Glutathione was 1.98 ± 0.13 μmol/g organ for glaucoma (controls 8.19 ± 0.71 μmol/g organ, p < 0.001). Superoxide dismutase and GPx were increased in glaucoma by 42 and 59%, respectively (p < 0.05).
  
  
  CONCLUSIONS
  Reactive oxygen and nitrogen species were increased in glaucoma, the increase in chemiluminescence, protein carbonylation and nitrite levels could be evidenced by this situation. The decrease in nonenzymatic antioxidants and a compensatory increase in SOD and GPx activity may have been a consequence of an increase in oxidative processes.
authors.affiliation: General and Inorganic Chemistry Division, School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina. smferrer@ffyb.uba.ar
authors.forename: Sandra M
authors.initials: SM
authors.lastname: Ferreira
authors.forename: Fabian
authors.initials: F
authors.lastname: Lerner
authors.forename: Claudia G
authors.initials: CG
authors.lastname: Reides
authors.forename: Ricardo
authors.initials: R
authors.lastname: Brunzini
authors.forename: Susana F
authors.initials: SF
authors.lastname: Llesuy
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000378:metabolism; D001921:Brain / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D007429:Intraocular Pressure; D049449:Luminescence; D009798:Ocular Hypertension / Q000378:metabolism*; D018384:Oxidative Stress; D050050:Protein Carbonylation; D051381:Rats; D017208:Rats, Wistar; D026361:Reactive Nitrogen Species / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D014810:Vitamin E / Q000378:metabolism
chemical_list: D000975:Antioxidants; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D014810:Vitamin E; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D001205:Ascorbic Acid