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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1994-5-17
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pubmed:abstractText |
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)
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Cations,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Pumps,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Rubidium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Selenite,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Potassium-Exchanging ATPase
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0014-4835
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
58
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
225-9
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:8157115-Animals,
pubmed-meshheading:8157115-Biological Transport, Active,
pubmed-meshheading:8157115-Calcium,
pubmed-meshheading:8157115-Cataract,
pubmed-meshheading:8157115-Cations,
pubmed-meshheading:8157115-Cell Membrane Permeability,
pubmed-meshheading:8157115-Ion Pumps,
pubmed-meshheading:8157115-Lens Capsule, Crystalline,
pubmed-meshheading:8157115-Membrane Proteins,
pubmed-meshheading:8157115-Rabbits,
pubmed-meshheading:8157115-Rubidium,
pubmed-meshheading:8157115-Sodium,
pubmed-meshheading:8157115-Sodium Selenite,
pubmed-meshheading:8157115-Sodium-Potassium-Exchanging ATPase,
pubmed-meshheading:8157115-Time Factors
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pubmed:year |
1994
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pubmed:articleTitle |
Selenite-induced damage to lens membranes.
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pubmed:affiliation |
Eye Research Institute, Oakland University, Rochester, MI 48309-4401.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.
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