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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1992-7-28
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pubmed:abstractText |
Repletion with Ca2+ often leads to damage of previously Ca(2+)-depleted hearts (the calcium paradox). The behavior of the liver under similar conditions is not well understood. With a perfused rat liver model, we examined liver cell damage and lipid peroxidation during Ca2+ depletion and repletion and used lucigenin-enhanced chemiluminescence as a measure of oxygen radicals. During 30 minutes of Ca2+ depletion, release of lactate dehydrogenase and thiobarbituric acid-reactive substance did not change significantly. When Ca2+ depletion was extended to 150 minutes, release of lactic acid dehydrogenase and thiobarbituric acid-reactive substance and tissue oxygen radical levels all increased progressively, accompanied by decrease in oxygen uptake. Ca2+ repletion after 30 minutes of Ca2+ depletion caused small increases in release of lactic acid dehydrogenase and thiobarbituric acid-reactive substance but significantly suppressed the changes described, compared with expression in depleted livers without Ca2+ repletion. There were large releases of sinusoidal glutathione and glutathione disulfide at the onset of Ca2+ depletion, which declined within 15 minutes. On Ca2+ repletion, sinusoidal glutathione level decreased to its baseline but glutathione disulfide level did not change significantly. During long-term Ca2+ depletion, sinusoidal glutathione level was significantly higher than baseline but glutathione disulfide level remained low. These results indicate that long-term Ca2+ depletion causes oxidative stress and liver damage. Ca(2+)-dependent release of sinusoidal glutathione appears to result from causes other than oxidative stress. There is no evidence for the calcium paradox in the liver; in fact, reexposure to Ca2+ protects the liver from the injury caused by Ca2+ depletion.
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pubmed:grant | |
pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione Disulfide,
http://linkedlifedata.com/resource/pubmed/chemical/L-Lactate Dehydrogenase,
http://linkedlifedata.com/resource/pubmed/chemical/Thiobarbiturates
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0022-2143
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
120
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
57-66
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1613329-Animals,
pubmed-meshheading:1613329-Calcium,
pubmed-meshheading:1613329-Glutathione,
pubmed-meshheading:1613329-Glutathione Disulfide,
pubmed-meshheading:1613329-L-Lactate Dehydrogenase,
pubmed-meshheading:1613329-Lipid Peroxidation,
pubmed-meshheading:1613329-Liver,
pubmed-meshheading:1613329-Luminescent Measurements,
pubmed-meshheading:1613329-Male,
pubmed-meshheading:1613329-Oxidation-Reduction,
pubmed-meshheading:1613329-Perfusion,
pubmed-meshheading:1613329-Rats,
pubmed-meshheading:1613329-Rats, Inbred Strains,
pubmed-meshheading:1613329-Thiobarbiturates,
pubmed-meshheading:1613329-Time Factors
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pubmed:year |
1992
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pubmed:articleTitle |
Depletion and repletion of Ca2+ in the perfused rat liver.
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pubmed:affiliation |
Department of Biochemistry and Biophysics, University of Pennsylvania, School of Medicine, Philadelphia 19104-6089.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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