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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1993-1-12
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pubmed:abstractText |
Perfusion of rat liver with Ca(2+)-depleted buffer induces oxidative stress and liver damage, which can be prevented by Ca2+ repletion (Okuda et al. J Lab Clin Med). In the present study, we investigated the action of ruthenium red on acute Ca2+ loading after Ca2+ depletion in the isolated perfused rat liver. The major findings of this study are that 1) Ca2+ depletion-induced liver damage was related to mitochondrial disfunction; 2) ruthenium red inhibited the oxidative stress and liver damage normally seen during Ca2+ depletion; 3) ruthenium red inhibited the Ca2+ depletion-induced mitochondrial disfunction. These observations suggest that mitochondrial Ca2+ cycling is responsible for Ca2+ depletion-induced oxidative stress and liver damage.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0034-5164
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
78
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
17-25
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1281333-Animals,
pubmed-meshheading:1281333-Calcium,
pubmed-meshheading:1281333-L-Lactate Dehydrogenase,
pubmed-meshheading:1281333-Liver,
pubmed-meshheading:1281333-Male,
pubmed-meshheading:1281333-Mitochondria, Liver,
pubmed-meshheading:1281333-Oxygen Consumption,
pubmed-meshheading:1281333-Perfusion,
pubmed-meshheading:1281333-Rats,
pubmed-meshheading:1281333-Rats, Sprague-Dawley,
pubmed-meshheading:1281333-Reperfusion Injury,
pubmed-meshheading:1281333-Ruthenium Red,
pubmed-meshheading:1281333-Thiobarbituric Acid Reactive Substances
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pubmed:year |
1992
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pubmed:articleTitle |
The effect of ruthenium red during Ca2+ depletion and repletion in the isolated 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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