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Sandra M Ferreira, Romina M. Lasagni Vitar, Fabian S Lerner, Agustina Peverini, Ricardo Brunzini, Claudia Reides, Susana Llesuy; Lipoic acid protects brain from oxidative damage in a glaucoma rat model. Invest. Ophthalmol. Vis. Sci. 2016;57(12):2563.
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© ARVO (1962-2015); The Authors (2016-present)
Glaucoma produces alterations in oxidative stress markers in brain. The use of an antioxidant therapy may hold a promise for treatment. The aim of this study was to evaluate the possible protective role of lipoic acid in oxidative damage of visual cortex in an experimental glaucoma model.
Rats were divided in four groups (n=16): glaucoma (G), glaucoma treated with lipoic acid 100 mg/kg i.p. (LG), control received a sham procedure (C), control treated with lipoic acid 100 mg/kg i.p. (LC). Episcleral venous occlusion model in Wistar rats (3 months) was used and 7 days after surgery were euthanized. Brains were removed and visual cortex was separated. These parameters were evaluated: thioredoxin reductase (TR), glutathione peroxidase (GPx), glutathione reductase (GR) and superoxide dismutase (SOD) activities, damage to lipids (TBARS), protein oxidation (PO), total non-enzymatic antioxidants (TRAP) and nitrite levels (NO). The statistical analyses were one-way ANOVA and a post hoc Tukey test.
Comparing glaucoma group to control group: TR diminished 34 % (14.9 ± 1.0 nmol/ min.mg protein p< 0.05), GPx increased 62 % (7.61± 0.75 nmol/ min.mg protein p< 0.05), GR decreased 61 % (13.0 ± 1.5 nmol/ min.mg protein p< 0.05), PO increased 138% (3.9 ± 0.1 nmol/ mg protein p<0.05), TRAP decreased 50 % (11.7 ± 1.0 nmol/ mg protein p<0.01), NO increased 47 % (2.37 ± 0.12 nmol/ mg protein p<0.05). TBARS increased 133 % ( 2.26 ± 0.23 nmol/ mg protein p<0.001).No significant changes were found in SOD.Comparing lipoic acid treated glaucoma group to glaucoma group: GR increased 300 % (5.14 ± 1.70 nmol/ min.mg protein p< 0.001), SOD increased 79 % (7.02 ± 0.45 U/ mg protein p<0.001), PO diminished 58% (9.34 ± 1.30 nmol/ mg protein p<0.05), TRAP increased 108 % (5.80 ± 0.48 nmol/ mg protein p<0.01), NO decreased 36 % (3.50 ± 0.28 nmol/ mg protein p<0.05). No significant changes were found in TBARS, GPx and TR.
Glaucoma induces an increase in prooxidants, a decay in non-enzymatic antioxidants, an increase in protein and lipid damage and a deficient GSH recycling. The protective role of lipoic acid in oxidative damage in glaucoma could be evidenced by the increase in non-enzymatic antioxidants and in the activities of antioxidant enzymes. Moreover, the decay in prooxidant species and the improvement in GSH recycling support that lipoc acid could be used as a novel therapy for reducing oxidative damage in glaucoma.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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