Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 40, Issue 9, Pages 1628-1635Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2005.12.033
Keywords
thyroid hormone; oxidative stress; liver; Kupffer cells; interleukin-6; signal transducer and activator of transcription 3; acute phase response; free radicals
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Recently, we reported that 3,3,5-triiodothyronine (T-3) induces the expression of redox-sensitive genes as a nongenomic mechanism of T3 action. In this study, we show that T3 administration to rats (daily doses of 0. 1 mg/kg ip for 3 consecutive days) induced a calorigenic response and liver glutathione depletion as an indication of oxidative stress, with higher levels of interleukin (IL)-6 in serum (ELISA) and hepatic STAT3 DNA binding (EMSA), which were maximal at 48-72 h after treatment. Under these conditions, the protein expression of the acute-phase proteins haptoglobin and beta-fibrinogen is significantly augmented, a change that is suppressed by pretreatment with a.-tocopherol (100 mg/kg ip) or gadolinium chloride (10 mg/kg iv) before T-3. It is concluded that T3 administration induces the acute-phase response in rat liver by a redox mechanism triggered at the Kupffer cell level, in association with IL-6 release and activation of the STAT3 cascade, a response that may contribute to reestablishing homeostasis in the liver and extrahepatic tissues exhibiting oxidative stress. (c) 2006 Elsevier Inc. All rights reserved.
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