Lipid peroxidation has been shown to be involved in the pathogenesis of some types of cataract. The possibility of such a mechanism was investigated in Emory mouse cataract. Malondi aldehyde, a breakdown product of lipid peroxides, increased 4-fold in advanced cataract. Studies on cation transport revealed that in early cataract there was no alteration in permeability and active transport of cations. However, these functions were significantly altered in advanced cataract as evidenced by about 300% increase in cellular influx of22Na+(140 mM) and 50% fall in cellular uptake of86Rb+(5 mM). At this stage of cataract, the ouabain- inhibitable component of uptake of Rb+was drastically decreased, whereas the ouabain-resistant component was unchanged. The mannitol-space increased markedly with progression of cataract. Altered transport of cations in cataract was indicative of damaged membranes which may be due to peroxidation of unsaturated fatty acids in the lipid bilayers concomitant with oxidation of sulfhydryl groups of proteins of the plasma membrane. Superoxide dismutase, catalase and glutathione peroxidase, the defensive enzymes against reactive species of oxygen, were decreased 54%, 57% and 62% respectively in cataract, exposing the lens to oxidants such as O2−, H2O2, OH and1ΔgO2, which can initiate lipid peroxidation and/or oxidation of protein.