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S. M. Ferreira, F. Lerner, R. Brunzini, C. G. Reides, S. F. Llesuy; Glaucoma Damage Beyond the Eye: Oxidative Stress Markers in Brain Homogenates. Invest. Ophthalmol. Vis. Sci. 2010;51(13):6108.
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© ARVO (1962-2015); The Authors (2016-present)
The aim of the present study was to establish the antioxidant status in brain homogenates of an experimental glaucoma model.
Wistar rats (n=8) were operated under a microscope by cauterized two of the episcleral veins (GG) while other control group (n=9) received a sham procedure (CG). In order to assess the occurrence of oxidative stress the following markers were evaluated in brain homogenates at seven days after the surgery: spontaneous chemiluminescence (CL), the activities of antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX), protein carbonylation (PC), ascorbic acid (AA), vitamin E (VE), gluthathione (GSH), and nitrite concentrations (NC). CL and TRAP were measured by chemiluminescence. The activity of the antioxidant enzymes, PO, NC concentration and the non-enzymatic antioxidants were measured spectrophotometrically.
CL in GG was 690 ± 41 cpm/mg protein (CG: 432 ± 29 cpm/ mg protein *p< 0.001). PC in glaucoma rats was 2.84 ± 0.216 nmoles/ mg protein (GC: 1.46 ± 0.27 nmoles/ mg protein *p< 0.001). SOD activity in GG was 3.98 ± 0.43 U/mg protein (CG 2.51 ± 0.28 U/mg protein *p< 0.05). GPX activity in glaucoma rats was 0.067 ± 0.008 U/mg protein.min (CG 0.042 ± 0.003 U/mg protein.min *p< 0.05). No significant changes were found in CAT. AA concentration was for GG 67 ± 26 µM (CG 275 ± 22 µM *p<0.001). VE concentration was 0.58 ± 0.05 µmol/g organ for GG (CG 1.10 ± 0.06 µmol/g organ *p< 0.01). GSH concentration was 1.98 ± 0.13 µmol/g organ for GG (CG 8.19 ± 0.71 µmol/g organ *p< 0.001). NC was 5.30 ± 0.25 µM for GG (CG 4.41 ± 0.24 µM *p< 0.05).
Reactive oxygen and nitrogen species were increased in glaucoma, this could be evidenced by the increased in the chemiluminescence, protein carbonylation and nitrite concentration. The decrease in non-enzymatic antioxidants and a compensatory up-regulation of SOD and glutathione peroxidase activity may be a consequence of an increase in oxidative process.
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