IBIMOL   23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
artículos
Título:
Brain antioxidant status in a high pressure-induced rat model of glaucoma.
Autor/es:
FERREIRA SM; LERNER F; REIDES CG; BRUNZINI R; LLESUY SF
Revista:
ACTA OPHTHALMOLOGICA
Editorial:
WILEY-BLACKWELL PUBLISHING, INC
Referencias:
Lugar: Londres; Año: 2013 vol. 91 p. 64 - 70
ISSN:
1755-375X
Resumen:
PURPOSE: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.