Lens calcium homeostasis and selenite cataract

A 3- to 5-fold increase in Ca2+ accompanies cataract formation induced by selenite. The mechanism of selenite cataractogenesis involves calcium activation of calpain with subsequent proteolysis within the lens nucleus. This study was undertaken to investigate the biochemical mechanisms that lead to calcium accumulation in these circumstances. The components responsible for rat lens calcium regulation were defined by using either lens membrane vesicle preparations or intact lenses. Both Na+ gradient-dependent Ca2+ uptake and efflux occurred in lens membrane vesicles. Experiments with intact lenses showed that Na + ICa2 + exchange plays an important role in lens calcium regulation. ATP-dependent Ca2+ uptake and Ca2+ -dependent ATP hydrolytic activity have been characterized in lens membrane vesicles. Therefore, both Ca2+ -ATPase and Na + ICa2+ exchange participate in rat lens calcium regulation. Calcium accumulation in lenses treated by selenite may result from either increased influx (via non-selective cation channel), decreased efflux (via Ca2 +-ATPase and Na+ ICa 2+ exchange) or both. The selenite effects on the different components involved in lens calcium regulation were tested.