It is known that oxidative stress leads to a number of well-characterized structural modifications in lens crystallins. These modified lens proteins accumulate within the lens and may play a major role in formation of some senile cataracts. We have proposed that singlet oxygen produced photodynamically may account for the oxidative damage. We have shown that photosensitizers endogenous to the lens can support the process, as could photosensitizing drugs which reach the lens. We have recently been able to extend studies of possible oxidative mechanisms of cataractogenesis to cataracts associated with chronic uveitis and retinal degenerative diseases respectively. In the first case, the lens is exposed to macrophages which are known to produce active species of oxygen, particularly hydrogen peroxide and superoxide. Cultured lenses are damaged when exposed to activated macrophages, apparently by an oxidative mechanism. In the case of cataracts associated with retinal degeneration we believe that peroxidation of the polyunsaturated lipids from degenerating rod outer segments may generate toxic species which initiate cataract.