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