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dc.creatorFERNÁNDEZ,VIRGINIA
dc.creatorTAPIA,GLADYS
dc.creatorVARELA,PATRICIA
dc.creatorCORNEJO,PAMELA
dc.creatorVIDELA,LUIS A
dc.date2009-01-01
dc.date.accessioned2019-05-02T21:21:52Z
dc.date.available2019-05-02T21:21:52Z
dc.identifierhttps://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0716-97602009000400010
dc.identifier.urihttp://revistaschilenas.uchile.cl/handle/2250/81992
dc.description3,3-5-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.
dc.formattext/html
dc.languageen
dc.publisherSociedad de Biología de Chile
dc.relation10.4067/S0716-97602009000400010
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceBiological Research v.42 n.4 2009
dc.subjectthyroid hormone
dc.subjectoxidative stress
dc.subjectinducible nitric oxide synthase
dc.subjectliver preconditioning
dc.subjectischemia-reperfusion injury
dc.subjectN-acetylcysteine
dc.titleUpregulation of liver inducible nitric oxide synthase following thyroid hormone preconditioning: suppression by N-acetylcysteine


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