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Molecular and Clinical Pharmacology Program and
¹ Cellular and Molecular Biology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Casilla 70000, Santiago-7, Chile

(Requests for offprints should be addressed to V Fernández; Email: vfernand{at}med.uchile.cl)

Recently, we demonstrated that 3,3',5-triiodothyronine (T3) induces oxidative stress in rat liver, with enhancement in the DNA binding of nuclear factor-B (NF-B) and the NF-B-dependent expression of tumor necrosis factor- (TNF-). In this study, we show that T3 administration (daily doses of 0.1 mg/kg i.p. for three consecutive days) elicited a calorigenic response and higher liver O₂ consumption rates, with increased serum levels of TNF- (ELISA), liver inhibitor of B (IB-) phosphorylation (Western blot analysis), and hepatic NF-B DNA binding (EMSA) at 56–72 h after treatment. Within this time interval, liver manganese superoxide dismutase (MnSOD) activity and the protein expression of MnSOD and Bcl-2 are enhanced. These changes are abrogated by the administration of -tocopherol (100 mg/kg i.p.) prior to T3. It is concluded that T3 treatment leads to the redox upregulation of MnSOD and Bcl-2 in rat liver, in association with TNF- release and activation of the IB- kinase/NF-B cascade, which may constitute a protective mechanism against free radical toxicity involving cell death signaling.