Selenite-induced damage to lens membranes

The present study focuses on three aspects of membrane damage to explain selenite-induced loss of ion homeostasis: membrane transport processes, i.e. cation pump; biosynthesis of membrane proteins and membrane permeability. Cation pump activity, assessed by both 86Rb uptake and Na-K-ATPase activity in the epithelium, was observed to decline gradually after exposure to selenite and subsequent culture for 2 days in a selenite-free medium. In fact, the major loss of transport and ATPase activity occurred during culture of lenses after transfer from selenite to a selenite-free medium. The delay between selenite presentation to the lens and final inhibition of the cation pump (47%) corresponds to the delay in the observed loss of Na-K-ATPase activity (50%). Initial loss of cation transport and Na-K-ATPase activity may be due to the oxidative capacity of selenite. Oxidation, however, might not explain the delayed, progressive loss of transport activity after selenite removal. A plausible cause for this sustained loss might be a depleted supply of Na-K-ATPase due to impaired biosynthesis. Evidence for such a possibility comes from the observation that the rate of synthesis of total membrane protein is impaired by 44% in selenite-treated lenses. Membrane permeability to Na+ was not affected at the end of day 1, a conclusion based on the following observation: ouabain-treated lenses exposed to selenite did not gain any more Na+ than did ouabain-treated lenses. With the pump blocked by ouabain in both groups of lenses, the passive influx of Na+ was unchanged by selenite, indicating little damage to membrane permeability.(ABSTRACT TRUNCATED AT 250 WORDS)