title: Selenite-induced damage to lens membranes.
abstract: 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)
authors.affiliation: Eye Research Institute, Oakland University, Rochester, MI 48309-4401.
authors.forename: K
authors.initials: K
authors.lastname: Hightower
authors.forename: J
authors.initials: J
authors.lastname: McCready
mesh_terms: D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000378:metabolism; D002386:Cataract / Q000139:chemically induced*; D002412:Cations / Q000378:metabolism; D002463:Cell Membrane Permeability / Q000187:drug effects; D066298:In Vitro Techniques; D016623:Ion Pumps / Q000187:drug effects; D007903:Lens Capsule, Crystalline / Q000378:metabolism*; D008565:Membrane Proteins / Q000096:biosynthesis; D011817:Rabbits; D012413:Rubidium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D018038:Sodium Selenite / Q000633:toxicity*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013997:Time Factors
chemical_list: D002412:Cations; D016623:Ion Pumps; D008565:Membrane Proteins; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D018038:Sodium Selenite; D012413:Rubidium; D002118:Calcium