| 18314881 |
Demori I, Burlando B, Gerdoni E, Lanni A, Fugassa E, Voci A: Uncoupling protein-2 induction in rat hepatocytes after acute carbon tetrachloride liver injury. J Cell Physiol. 2008 Aug;216(2):413-8.
This study is focused on the role of UCP-2 in hepatic oxidative metabolism following acute CCl (4) administration to rats. UCP-2 mRNA, almost undetectable in the liver of controls, was significantly increased 24 h after CCl (4) administration, peaked at 72 h and then tended to disappear. UCP-2 protein, undetectable in controls, increased 48-72 h after CCl (4) treatment. Experiments with isolated liver cells indicated that in control rats UCP-2 was expressed in non-parenchymal cells and not in hepatocytes, whereas in CCl (4)-treated rats UCP-2 expression was induced in hepatocytes and was not affected in non-parenchymal cells. Addition of CCl (4) to the culture medium of hepatocytes from control rats failed to induce UCP-2 expression. Liver mitochondria from CCl (4)-treated rats showed an increase of H (2) O (2) release at 12-24 h, followed by a rise of TBARS. Vitamin E protected liver from CCl (4) injury and reduced the expression of UCP-2. Treatment with GdCl (3) prior to CCl (4), in order to inhibit Kupffer cells, reduced TBARS and UCP-2 mRNA increase in hepatic mitochondria. Our data indicate that CCl (4) induces the expression of UCP-2 in hepatocytes with a redox-dependent mechanism involving Kupffer cells. A role of UCP-2 in moderating CCl (4)-induced oxidative stress during tissue regeneration after injury is suggested. |
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