| pubmed-article:3996400 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3996400 | lifeskim:mentions | umls-concept:C1882726 | lld:lifeskim |
| pubmed-article:3996400 | lifeskim:mentions | umls-concept:C0025270 | lld:lifeskim |
| pubmed-article:3996400 | lifeskim:mentions | umls-concept:C0205409 | lld:lifeskim |
| pubmed-article:3996400 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:3996400 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:3996400 | lifeskim:mentions | umls-concept:C1511636 | lld:lifeskim |
| pubmed-article:3996400 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:3996400 | lifeskim:mentions | umls-concept:C1549542 | lld:lifeskim |
| pubmed-article:3996400 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:3996400 | pubmed:dateCreated | 1985-7-17 | lld:pubmed |
| pubmed-article:3996400 | pubmed:abstractText | Previous studies have indicated that the presence of cytotoxic levels of menadione (2-methyl-1,4-naphthoquinone) causes rapid changes in intracellular thiol and Ca2+ homeostasis in isolated rat hepatocytes. The present investigation was undertaken to examine these effects in the intact liver. Rat livers were therefore perfused with Krebs-Henseleit buffer containing 1.3 mM Ca2+ using a single-pass mode, and the perfusate Ca2+ level was monitored with an on-line Ca2+-selective electrode. Infusion of menadione elicited an increased O2 uptake by the liver, followed by a dose-dependent decrease in the perfusate level of Ca2+. Hepatic accumulation of Ca2+ was accompanied by stimulation of cytosolic phosphorylase a activity. Cessation of menadione infusion resulted in gradual recovery of perfusate Ca2+ to base levels. Ca2+ uptake was not accompanied by decreases in reduced pyridine nucleotide or ATP levels in the liver as evidenced by measurements either during maximal Ca2+ uptake or after recovery. However, Ca2+ uptake was correlated with decreased glutathione and increased glutathione disulfide levels in the liver, both of which reversed during recovery from Ca2+ uptake. Moreover, depletion of hepatic glutathione by pretreatment with diethylmaleate resulted in increased Ca2+ uptake during menadione infusion. The amount of protein-bound mixed disulfides showed a particularly striking relationship to Ca2+ uptake, reaching a maximal level during Ca2+ uptake and reversing toward normal value during recovery from Ca2+ accumulation. The present findings suggest that menadione-induced Ca2+ uptake is due to plasma membrane dysfunction as a result of loss of protein thiol groups critical for maintaining the plasma membrane Ca2+ extrusion mechanism. Our model offers a particularly useful opportunity to study mechanisms underlying toxic disturbances in Ca2+ homeostasis in the intact liver, since Ca2+ fluxes can be monitored under conditions in which cellular control mechanisms are not obliterated by excessive toxicity. | lld:pubmed |
| pubmed-article:3996400 | pubmed:language | eng | lld:pubmed |
| pubmed-article:3996400 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3996400 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:3996400 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3996400 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3996400 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3996400 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3996400 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3996400 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3996400 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3996400 | pubmed:month | May | lld:pubmed |
| pubmed-article:3996400 | pubmed:issn | 0014-2956 | lld:pubmed |
| pubmed-article:3996400 | pubmed:author | pubmed-author:MehendaleH... | lld:pubmed |
| pubmed-article:3996400 | pubmed:author | pubmed-author:OrreniusSS | lld:pubmed |
| pubmed-article:3996400 | pubmed:author | pubmed-author:BaldiCC | lld:pubmed |
| pubmed-article:3996400 | pubmed:author | pubmed-author:SvenssonS ASA | lld:pubmed |
| pubmed-article:3996400 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3996400 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:3996400 | pubmed:volume | 149 | lld:pubmed |
| pubmed-article:3996400 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3996400 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3996400 | pubmed:pagination | 201-6 | lld:pubmed |
| pubmed-article:3996400 | pubmed:dateRevised | 2007-7-23 | lld:pubmed |
| pubmed-article:3996400 | pubmed:meshHeading | pubmed-meshheading:3996400-... | lld:pubmed |
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| pubmed-article:3996400 | pubmed:meshHeading | pubmed-meshheading:3996400-... | lld:pubmed |
| pubmed-article:3996400 | pubmed:year | 1985 | lld:pubmed |
| pubmed-article:3996400 | pubmed:articleTitle | Accumulation of Ca2+ induced by cytotoxic levels of menadione in the isolated, perfused rat liver. | lld:pubmed |
| pubmed-article:3996400 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3996400 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:3996400 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:3996400 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:3996400 | lld:pubmed |
