|Thyroid hormone (TH; 3,3,,5-triiodothyronine, T-3) is required for the normal function of most tissues, with major effects on O-2 consumption and metabolic rate. These are due to transcriptional activation of respiratory genes through the interaction of T-3-liganded TH receptors with TH response elements or the activation of intermediate factors, with the consequent higher production of reactive O-2 species (ROS) and antioxidant depletion. T-3-induced oxidative stress in the liver triggers the redox upregulation of the expression of cytokines (tumor necrosis factor-alpha [TNF-alpha], interleukin- 10), enzymes (inducible nitric oxide synthase, manganese superoxide dismutase), and anti-apoptotic proteins (Bcl-2), via a cascade initiated by TNF-alpha produced by Kupffer cells, involving inhibitor of kappa B phosphorylation and nuclear factor-kappa B activation. Thus, TH calorigenesis triggers an expression pattern that may represent an adaptive mechanism to re-establish redox homeostasis and promote cell survival under conditions of ROS toxicity secondary to TH-induced oxidative stress. Mechanisms of expression of respiratory and redox-sensitive genes may be functionally integrated, which could be of importance to understand the complexities of TH action and the outcome of thyroid gland dysfunction.