Open Access

ARTICLE

Changes in the redox status of the brain in an experimental glaucoma model

Claudia G. REIDES^1,2, Romina M. LASAGNI VITAR^1,2, Agustina PEVERINI¹, Natasha S. JANEZIC¹, Ailen G. HVOZDA ARANA¹, Sandra M. FERREIRA^1,2, Susana F. LLESUY^1,2*

1 Química General e Inorgánica, Facultad de Farmacia y Bioquímica. Universidad de Buenos Aires, Buenos Aires Argentina.
2 Instituto de Bioquímica y Medicina Molecular (IBIMOL), Universidad de Buenos Aires-CONICET, Buenos Aires, Argentina.

* Address correspondence to: Susana Llesuy,

BIOCELL 2016, 40(1), 51-54. https://doi.org/10.32604/biocell.2016.40.051

Abstract

The purpose of this study was to evaluate the redox status changes of primary visual targets in the rat brain of a high pressure-induced glaucoma model. The animal model consisted of inducing ocular hypertension by cauterizing two episcleral veins on the left eye. The markers of oxidative damage and the oxidative balance evaluated in the brain seven days postoperative were: nitrites concentration, levels of non-enzymatic antioxidants and antioxidant enzymes activity.
The increase in the nitrite content, which could be the result of the enhancement in the production of nitrogen species, and in the activity of NADPH oxidase in the glaucoma group could lead to an increase on lipid and protein damage.
The decrease on the non-enzymatic antioxidants and the compensatory increase of the superoxide dismutase and glutathione peroxidase activities could be a consequence of the increase of oxidative processes. The decrease in the activity of glutathione reductase leads to a decrease in the recycling of thiol groups.
We suggest that oxidative stress can possibly acts as a risk factor for neurodegeneration in the brain. Therapeutic strategies to stop the progression of the disease in glaucoma should also be considered the central neuronal degeneration beyond the retina and the optic nerve.

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Keywords

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