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UCP\u20102 mRNA, almost undetectable in the liver of controls, was significantly increased 24 h after CCl<jats:sub>4<\/jats:sub> administration, peaked at 72 h and then tended to disappear. UCP\u20102 protein, undetectable in controls, increased 48\u201372 h after CCl<jats:sub>4<\/jats:sub> treatment. Experiments with isolated liver cells indicated that in control rats UCP\u20102 was expressed in non\u2010parenchymal cells and not in hepatocytes, whereas in CCl<jats:sub>4<\/jats:sub>\u2010treated rats UCP\u20102 expression was induced in hepatocytes and was not affected in non\u2010parenchymal cells. Addition of CCl<jats:sub>4<\/jats:sub> to the culture medium of hepatocytes from control rats failed to induce UCP\u20102 expression. Liver mitochondria from CCl<jats:sub>4<\/jats:sub>\u2010treated rats showed an increase of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> release at 12\u201324 h, followed by a rise of TBARS. Vitamin E protected liver from CCl<jats:sub>4<\/jats:sub> injury and reduced the expression of UCP\u20102. Treatment with GdCl<jats:sub>3<\/jats:sub> prior to CCl<jats:sub>4<\/jats:sub>, in order to inhibit Kupffer cells, reduced TBARS and UCP\u20102 mRNA increase in hepatic mitochondria. Our data indicate that CCl<jats:sub>4<\/jats:sub> induces the expression of UCP\u20102 in hepatocytes with a redox\u2010dependent mechanism involving Kupffer cells. A role of UCP\u20102 in moderating CCl<jats:sub>4<\/jats:sub>\u2010induced oxidative stress during tissue regeneration after injury is suggested. J. Cell. Physiol. 216: 413\u2013418, 2008. \u00a9 2008 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.21415","type":"journal-article","created":{"date-parts":[[2008,3,3]],"date-time":"2008-03-03T18:21:15Z","timestamp":1204568475000},"page":"413-418","source":"Crossref","is-referenced-by-count":6,"title":["Uncoupling protein\u20102 induction in rat hepatocytes after acute carbon tetrachloride liver 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