Cholesterol and lipid peroxidation in 3 beta-(2-diethylaminoethoxy)- androst-5-en-17-oneHCl (U18666A) induced cataractogenesis in rats.

Decrease in cholesterol was observed in precataractous, cataractous, advance nuclear cataractous and non-cataractous lenses when 3 beta-(2-diethylaminoethoxy)-androst-5-en-17- oneHCl (U18666A) was injected, sc, to rats. Significant increase in lipid peroxidation was observed before the onset of any apparent lenticular opacity in U18666A treated rats. The results suggest that decrease in cholesterol is capable of altering the structural integrity of lens fibers. However, 12.5% decrease in cholesterol and 5% increase in lipid peroxidation observed in non-cataractous lenses indicated that these changes are not sufficient for any apparent opacification.