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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.