Hepatic nitrosative stress in experimental diabetes

Curso de Fisioterapia/Centro de Ciências da Vida e da saúde - Universidade Católica de Pelotas (UCPEL) 96010-000, Pelotas, RS, Brazil.
Journal of diabetes and its complications (Impact Factor: 3.01). 06/2012; 26(5):378-81. DOI: 10.1016/j.jdiacomp.2012.04.015
Source: PubMed


The effects of the inhibition of nitrosative stress by aminoguanidine in an experimental model of diabetes mellitus (DM) were investigated.
Twenty-one male Wistar rats were divided into three groups: control (CO), diabetic (DM), and diabetic treated with aminoguanidine (DM+AG). Aminoguanidine (aminoguanidine hemisulfate salt, Sigma Chemical Co., St. Louis, MO, USA) was used at a dose of 50mg/kg (i.p.) during the last 30days of the experiment. The expression levels of liver lipoperoxidation (TBARS - nmol/mg protein), inducible oxide nitric synthase (iNOS), nitrotyrosine and the NFκB nuclear transcription factor p65 were examined using western blot analysis.
The DM group demonstrated an increase in lipoperoxidation and in the expression of iNOS, nitrotyrosine and p65. Aminoguanidine reduced hepatic lipid peroxidation and protein expression levels of iNOS, nitrotyrosine and p65.
Aminoguanidine treatment reduces liver oxidative and nitrosative stress in diabetic animals. In addition, aminoguanidine reduced the expression of p65 in the liver.

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    • "Another interesting result of the present study is the self protection of liver in case of aging and diabetes against an increase in the levels of 3-NT, however 3-NT was significantly propagated by aging and diabetes in other studied tissues. This finding is supported by our previous study demonstrating that liver 3-NT levels were unaffected by diabetes or stobadine treatment in comparison with normal control rats (Cumaoglu et al., 2007), while others demonstrated an increase in the expression of hepatic iNOS and nitrotyrosine in animal model of diabetes (Di Naso et al., 2012). Superoxide anion reacts with NO to form highly toxic peroxynitrite and this could also account for the inactivation of NO in diabetic rats. "
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