da Silva, Carla B. P.
Ceron, Carla S.
Mendes, Atlante S.
de Martinis, Bruno S.
Castro, Michele M.
Tirapelli, Carlos R.
Total Authors: 6
 Univ Sao Paulo, Escola Enfermagem Ribeirao Preto, DEPCH, Lab Farmacol, Ribeirao Preto, SP - Brazil
 Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Programa Posgrad Toxicol, Ribeirao Preto, SP - Brazil
 Univ Fed Ouro Preto, Dept Ciencias Biol, Ouro Preto, MG - Brazil
 Univ Sao Paulo, Fac Med Ribeirao Preto, Ribeirao Preto, SP - Brazil
 Univ Sao Paulo, Fac Filosofia Ciencias & Letras Ribeirao Preto, Dept Quim, Ribeirao Preto, SP - Brazil
Total Affiliations: 5
Canadian Journal of Physiology and Pharmacology;
Web of Science Citations:
Overexpression of the inducible isoform of the enzyme nitric oxide synthase (iNOS) has been associated to pathological processes in the kidney. Ethanol consumption induces the renal expression of iNOS; however, the contribution of this enzyme to the deleterious effects of ethanol in the kidney remains elusive. We examined whether iNOS plays a role in the renal dysfunction and oxidative stress induced by ethanol consumption. With this purpose, male C57BL/6 wild-type (WI) or iNOS-deficient (iNOS(-/-)) mice were treated with ethanol (20% WO for 10 weeks. Treatment with ethanol increased the expression of Nox4 as well as the concentration of thiobarbituric acid reactive substances and the levels of tumor necrosis factor a in the renal cortex of ANT but not iNOS(-/-) mice. Augmented serum levels of creatinine and increased systolic blood pressure were found in ANT and iNOS(-/-) mice treated with ethanol. WT mice treated with ethanol showed increased production of reactive oxygen species and myeloperoxidase activity, but these responses were attenuated in iNOS(-/-) mice. We concluded that iNOS played a role in ethanol-induced oxidative stress and pro-inflammatory cytokine production in the kidney. These are mechanisms that may contribute to the renal toxicity induced by ethanol. (AU)