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Effects of g-hexachlorocyclohexane and L-3,3',5- triiodothyronine on rat liver cytochrome P4502E1- dependent activity and content in relation to microsomal superoxide radical generation Biol. Res.
FERNÁNDEZ,VIRGINIA; MASSA,LAURA; QUIÑONES,LUIS; SIMON-GIAVAROTTI,KARIN A; GIAVAROTTI,LEANDRO; D'ALMEIDA,VÂNIA; AZZALIS,LIGIA A; JUNQUEIRA,VIRGINIA BC; VIDELA,LUIS A.
Liver microsomal cytochrome P4502E1-dependent p-nitrophenol (PNP) hydroxylation and expression of cytochrome P4502E1 were studied in rats subjected to g-hexachlorocyclohexane (HCCH) or L-3,3,,5-triiodothyronine (T3) administration as a possible mechanism contributing to superoxide radical (O2.-) generation. HCCH treatment (a single dose of 40 mg/kg body wt) produced a 43% increase in the content of total cytochrome P450, whereas T3 (daily doses of 0.1 mg/kg body wt for two consecutive days) led to a 37% decrease. NADPH-dependent O2.- generation was elevated by HCCH and T3, expressed as either per mg of protein or per nmol of cytochrome P450, with a 135% enhancement in the O2.- production/superoxide dismutase (SOD) activity ratios being observed in both...
Tipo: Journal article Palavras-chave: G-Hexachlorocyclohexane L-3; 3'; 5-Triiodothyronine Superoxide radical Cytochrome P4502E1 Rat liver.
Ano: 2003 URL: http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602003000300007
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The role of thyroid hormone calorigenesis in the redox regulation of gene expression Biol. Res.
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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Upregulation of liver inducible nitric oxide synthase following thyroid hormone preconditioning: suppression by N-acetylcysteine Biol. Res.
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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