Upregulation of liver inducible nitric oxide synthase following thyroid hormone preconditioning: suppression by N-acetylcysteine

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...

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Autores principales:	FERNÁNDEZ,VIRGINIA, TAPIA,GLADYS, VARELA,PATRICIA, CORNEJO,PAMELA, VIDELA,LUIS A
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2009
Materias:	thyroid hormone oxidative stress inducible nitric oxide synthase liver preconditioning ischemia-reperfusion injury N-acetylcysteine
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602009000400010
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spelling	oai:scielo:S0716-976020090004000102010-03-17Upregulation of liver inducible nitric oxide synthase following thyroid hormone preconditioning: suppression by N-acetylcysteineFERNÁNDEZ,VIRGINIATAPIA,GLADYSVARELA,PATRICIACORNEJO,PAMELAVIDELA,LUIS A thyroid hormone oxidative stress inducible nitric oxide synthase liver preconditioning ischemia-reperfusion injury N-acetylcysteine 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 hepatic IR injury, with 119% enhancement in liver iNOS mRNA/18S rRNA ratios (p<0.05) and 12.7-fold increase (p<0.05) in NOS activity in T3-treated animals subjected to IR over values in control-sham operated rats, with a net 7.7-fold enhancement (p<0.05) in the net effect of T3 on liver iNOS expression and a net enhancement of 0.58 units in NOS activity, changes that were abolished by NAC treatment before T3. It is concluded that T3-induced liver PC is associated with upregulation of iNOS expression as a protective mechanisms against IR injury, which is achieved through development of transient and reversible oxidative stress.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.42 n.4 20092009-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602009000400010en10.4067/S0716-97602009000400010
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	thyroid hormone oxidative stress inducible nitric oxide synthase liver preconditioning ischemia-reperfusion injury N-acetylcysteine
spellingShingle	thyroid hormone oxidative stress inducible nitric oxide synthase liver preconditioning ischemia-reperfusion injury N-acetylcysteine FERNÁNDEZ,VIRGINIA TAPIA,GLADYS VARELA,PATRICIA CORNEJO,PAMELA VIDELA,LUIS A Upregulation of liver inducible nitric oxide synthase following thyroid hormone preconditioning: suppression by N-acetylcysteine
description	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 hepatic IR injury, with 119% enhancement in liver iNOS mRNA/18S rRNA ratios (p<0.05) and 12.7-fold increase (p<0.05) in NOS activity in T3-treated animals subjected to IR over values in control-sham operated rats, with a net 7.7-fold enhancement (p<0.05) in the net effect of T3 on liver iNOS expression and a net enhancement of 0.58 units in NOS activity, changes that were abolished by NAC treatment before T3. It is concluded that T3-induced liver PC is associated with upregulation of iNOS expression as a protective mechanisms against IR injury, which is achieved through development of transient and reversible oxidative stress.
author	FERNÁNDEZ,VIRGINIA TAPIA,GLADYS VARELA,PATRICIA CORNEJO,PAMELA VIDELA,LUIS A
author_facet	FERNÁNDEZ,VIRGINIA TAPIA,GLADYS VARELA,PATRICIA CORNEJO,PAMELA VIDELA,LUIS A
author_sort	FERNÁNDEZ,VIRGINIA
title	Upregulation of liver inducible nitric oxide synthase following thyroid hormone preconditioning: suppression by N-acetylcysteine
title_short	Upregulation of liver inducible nitric oxide synthase following thyroid hormone preconditioning: suppression by N-acetylcysteine
title_full	Upregulation of liver inducible nitric oxide synthase following thyroid hormone preconditioning: suppression by N-acetylcysteine
title_fullStr	Upregulation of liver inducible nitric oxide synthase following thyroid hormone preconditioning: suppression by N-acetylcysteine
title_full_unstemmed	Upregulation of liver inducible nitric oxide synthase following thyroid hormone preconditioning: suppression by N-acetylcysteine
title_sort	upregulation of liver inducible nitric oxide synthase following thyroid hormone preconditioning: suppression by n-acetylcysteine
publisher	Sociedad de Biología de Chile
publishDate	2009
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602009000400010
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_version_	1718441453248577536

Upregulation of liver inducible nitric oxide synthase following thyroid hormone preconditioning: suppression by N-acetylcysteine

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