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| VARELA,PATRICIA; TAPIA,GLADYS; FERNÁNDEZ,VIRGINIA; VIDELA,LUIS A. |
| Thyroid hormone (TH; 3,3',5-triiodothyronine, T3) is required for the normal function of most tissues, with major effects on 0(2) consumption and metabolic rate. These are due to transcriptional activation of respiratory genes through the interaction of T3-liganded TH receptors with TH response elements or the activation of intermediate factors, with the consequent higher production of reactive 0(2) species (ROS) and antioxidant depletion. T3-induced oxidative stress in the liver triggers the redox upregulation of the expression of cytokines (tumor necrosis factor-á [TNF-á], interleukin-10), enzymes (inducible nitric oxide synthase, manganese superoxide dismutase), and anti-apoptotic proteins (Bcl-2), via a cascade initiated by TNF-á produced by Kupffer... |
| Tipo: Journal article |
Palavras-chave: Thyroid hormone; Calorigenesis; Oxidative stress; Gene expression. |
| Ano: 2006 |
URL: http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602006000500004 |
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| FERNÁNDEZ,VIRGINIA; TAPIA,GLADYS; VARELA,PATRICIA; CORNEJO,PAMELA; VIDELA,LUIS A. |
| 3,3-5-L-Triiodothyronine (T3) exerts significant protection against ischemia-reperfusion (IR) liver injury in rats. Considering that the underlying mechanisms are unknown, the aim of this study was to assess the involvement of inducible nitric oxide synthase (iNOS) expression and oxidative stress in T3 preconditioning (PC). Male Sprague-Dawley rats given a single dose of 0.1 mg of T3/kg were subjected to 1-hour ischemia followed by 20 hours reperfusion, in groups of animals pretreated with 0.5 g of N-acetylcysteine (NAC)/kg 0.5-hour prior to T3 or with the respective control vehicles. At the end of the reperfusion period, liver samples were taken for analysis of iNOS mRNA levels (RT-PCR), liver NOS activity, and hepatic histology. T3 protected against... |
| Tipo: Journal article |
Palavras-chave: Thyroid hormone; Oxidative stress; Inducible nitric oxide synthase; Liver preconditioning; Ischemia-reperfusion injury; N-acetylcysteine. |
| Ano: 2009 |
URL: http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602009000400010 |
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