Inducible nitric oxide synthase (iNOS) mediates ethanol-induced redox imbalance and upregulation of inflammato cytokines in the kidney

Autor(es)

da Silva, Carla B. P. ^{[1, 2]} ; Ceron, Carla S. ^[3] ; Mendes, Atlante S. ^[4] ; de Martinis, Bruno S. ^[5] ; Castro, Michele M. ^[4] ; Tirapelli, Carlos R. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Escola Enfermagem Ribeirao Preto, DEPCH, Lab Farmacol, Ribeirao Preto, SP - Brazil

^[2] Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Programa Posgrad Toxicol, Ribeirao Preto, SP - Brazil

^[3] Univ Fed Ouro Preto, Dept Ciencias Biol, Ouro Preto, MG - Brazil

^[4] Univ Sao Paulo, Fac Med Ribeirao Preto, Ribeirao Preto, SP - Brazil

^[5] Univ Sao Paulo, Fac Filosofia Ciencias & Letras Ribeirao Preto, Dept Quim, Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Canadian Journal of Physiology and Pharmacology; v. 99, n. 10, p. 1016-1025, OCT 2021.
• Citações Web of Science: 0

Resumo

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)

• Processo FAPESP: 16/17623-9 - MECANISMOS DA TOXICIDADE RENAL INDUZIDA PELO CONSUMO CRÔNICO DE ETANOL: PAPEL DA ENZIMA ÓXIDO NÍTRICO SINTASE INDUZÍVEL (iNOS)
• Beneficiário: Carla Brigagão Pacheco da Silva
• Modalidade de apoio: Bolsas no Brasil - Doutorado