Senile cataracts and oxidative stress

In numerous epidemiological and animal models, it can be inferred that oxidative stress is a key factor in cataract formation. Production of reactive oxygen species and reduction of endogenous antioxidants both contribute to cataract formation. In the cataractogenous process, lens proteins lose sulfhydryl groups and become thiolated or cross-linked by disulfide bonds. The resultant high molecular weight aggregates become insoluble and affect lens transparency. All these are consequences of changes in the redox state. A mixed protein-thiol and protein-protein disulfide bond precedes the morphological changes of cataract. Normally, sustained high levels of reduced glutathione provide a protective effect, while depletion of glutathione causes damage to epithelial cells and fiber cells. UV rays in the ambient environment evoke reactive oxygen species formation and also contribute to cataracts. The reduction in free UV filters and increase in their binding to lens proteins make the lens more predisposed to UV damage and oxidation. In the aqueous humor of cataract lenses, there is a decrease in antioxidant enzymes and increase in nitric oxide, which demonstrates the relationship between oxidative stress and cataracts. Though surgical intervention is the standard treatment for cataracts, experimental medical therapies for cataracts are under extensive investigation. Carnosine, a pro-drug of carnosine-N-acetylcarnosine, bendazac, ascorbic acid, and aldose reductase inhibitors are under therapeutic evaluation, and prevention of cataract formation may be possible in the future.