Retinal oxidative stress induced by high intraocular pressure.

Free Radic Biol Med

Laboratorio de Neuroquímica Retiniana y Oftalmología Experimental, Departmento de Bioquímica Humana, Universidad de Buenos Aires, CONICET, Buenos Aires, Argentina.

Published: September 2004

AI Article Synopsis

  • Glaucoma is linked to the death of retinal ganglion cells, possibly through an apoptosis process fueled by oxidative stress, which involves free radicals.
  • The study examined the effects of chronic hyaluronic acid injections in rats and found decreased activity of key antioxidant enzymes in the retina over time, alongside increased oxidative damage indicators.
  • Results suggest that managing oxidative stress with antioxidants could be a potential treatment strategy to prevent cell death in glaucoma.

Article Abstract

Glaucoma is an optic neuropathy in which retinal ganglion cells die probably through an apoptotic process. Apoptosis is known to involve free radicals in several systems including the retina. In this context, the aim of the present work was to analyze retinal oxidative damage in rats with glaucoma induced by the chronic injection of hyaluronic acid in the eye anterior chamber. The results showed a significant decrease in total retinal superoxide dismutase and catalase activities after 6 and 3 weeks of treatment with hyaluronic acid, respectively. Also, although GPX activity increased after 10 weeks of ocular hypertension, GSH levels significantly decreased at 6 weeks of treatment with hyaluronic acid. Moreover, retinal lipid peroxidation significantly increased in a time-of-hypertension-dependent manner. On the other hand, a significant decrease in both diurnal and nocturnal retinal melatonin content was detected at 3, 6, or 10 weeks of treatment with hyaluronic acid. The present results suggest that retinal oxidative stress may be involved in glaucomatous cell death. Thus, manipulation of intracellular redox status using antioxidants may be a new therapeutic tool to prevent glaucomatous neurodegeneration.

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http://dx.doi.org/10.1016/j.freeradbiomed.2004.06.001DOI Listing

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