Calcium permeability was significantly increased in lenses from rats 36 h following a single injection of a cataractogenic dose of sodium selenite (30 nmol/g body weight) and this permeability returned to control values by 72 h post-injection (PI). The greater Ca2+permeability could be partially reversed by incubating lenses in medium containing 2 mM dithiothreitol (DTT). Estimations of Ca-ATPase activity revealed the greatest level occurred in the epithelial layer and that the nucleus had no detectable activity. By 48 h PI both Ca2+-pump activity and the Ca2+-dependent ATP hydrolytic activity were less compared to controls in membrane preparations from rat lenses. Only the hydrolytic activity could be partially restored by treatment with 5 mM DTT. Both permeability and active Ca2+transport were affected by selenite in a manner that would lead to increased Ca2+accumulation in lenses from rats treated with selenite. It is suggested that the oxidative damage that accompanies in vivo exposure to selenite could affect Ca2+homeostasis in the lens by directly altering permeability and Ca-ATPase.