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The role of thyroid hormone calorigenesis in the redox regulation of gene expression

Authordc.contributor.authorVarela, Patricia 
Authordc.contributor.authorTapia Opazo, Gladys es_CL
Authordc.contributor.authorFernández Arancibia, Virginia es_CL
Authordc.contributor.authorVidela Cabrera, Luis es_CL
Cita de ítemdc.identifier.citationBIOLOGICAL RESEARCH Volume: 39 Issue: 4 Pages: 611-617 Published: 2006en
Abstractdc.description.abstractThyroid 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.en
Publisherdc.publisherSOC BIOLGIA CHILEen
Títulodc.titleThe role of thyroid hormone calorigenesis in the redox regulation of gene expressionen
Document typedc.typeArtículo de revistaen

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