Early oxidation-related changes in aqueous humor following eye exposure to ultraviolet-A radiation.

Ultraviolet (UV) A represents 95% of the UV rays reaching the ocular surface. These rays exert their toxicity mainly via photosensitization reactions that generate oxidation and are implicated in various pathologies of the anterior segment of the eye. The cornea absorbs some UVA rays, but the majority passes through the aqueous humor (AH) to reach the lens. Previous work has mainly focused on understanding the consequences of UVA exposure on the cornea and lens, but the AH has been largely ignored. AH contains a high concentration of antioxidants and thus represents a key line of defense against oxidative stress in the anterior part of the eye. Using cadaveric rabbit eyes, we have evaluated the influence of ocular UVA exposure on oxidation in AH. Ocular exposure to UVA mediates the reduction of ascorbic acid levels in AH and results in a marked decrease in the reduced to oxidized glutathione (GSH/GSSG) ratio in AH, an increase in S-glutathionylated proteins (PSSG) content, and in the accumulation of toxic diffusible products such as malondialdehyde, a toxic by-product resulting from lipid peroxidation. These generated products can threaten the integrity of the trabecular meshwork during AH outflow or of structures in contact with AH such as the corneal endothelium or the lens. This work represents the first evidence that the toxicity of UVA to the eye can be mediated by its effect on AH. A better understanding of the effects induced by UVA on AH redox homeostasis is important if we want to better understand the risks associated with ocular UVA exposure.