@Article{biocell.2016.40.051,
AUTHOR = {Claudia G. REIDES, Romina M. LASAGNI VITAR, Agustina PEVERINI, Natasha S. JANEZIC, Ailen G. HVOZDA  ARANA, Sandra M. FERREIRA, Susana F. LLESUY},
TITLE = {Changes in the redox status of the brain in an experimental glaucoma model},
JOURNAL = {BIOCELL},
VOLUME = {40},
YEAR = {2016},
NUMBER = {1},
PAGES = {51--54},
URL = {http://www.techscience.com/biocell/v40n1/34018},
ISSN = {1667-5746},
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.<br/>
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.<br/>
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.<br/>
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.},
DOI = {10.32604/biocell.2016.40.051}
}