The past year has produced many advances in our knowledge of experimental and human cataract. Additional information on mechanisms of cataractogenesis has come from in vitro studies. Further investigations of anticataract therapy have been reported this year. Two major pathways to sugar cataract in rats, sorbitol formation and glycation, have been studied. The roles of malondialdehyde, lipid peroxidation, and calcium received further attention as did genetic and ultraviolet-induced cataract. Blood flow, glutathione, and lens proteins are altered in human cataract. Epidemiologic studies this year confirmed the enormous burden of cataract especially in the Third World, and have identified a variety of risk factors. Sugar cataracts in rats could be prevented not only by sorbitol-lowering drugs but also by aspirin, patacetamol, ibuprofen, and by myo-inositol. In humans, aspirin and ibuprofen were associated with protection against cataract, while bendazac was tested in a clinical trial.