Inducible nitric oxide synthase (iNOS) mediates ethanol-induced redox imbalance and upregulation of inflammatory cytokines in the kidney
| Autor: | Bruno De Martinis, Michele M. Castro, Carla Brigagão Pacheco da Silva, Carla Speroni Ceron, Atlante S. Mendes, Carlos R. Tirapelli |
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| Rok vydání: | 2021 |
| Předmět: |
Gene isoform
Male Alcohol Drinking Physiology Renal cortex Nitric Oxide Synthase Type II medicine.disease_cause Proinflammatory cytokine Mice Downregulation and upregulation Physiology (medical) medicine Animals Pharmacology chemistry.chemical_classification Inflammation Mice Knockout Kidney biology Ethanol Chemistry General Medicine Cell biology Nitric oxide synthase ESPÉCIES REATIVAS DE OXIGÊNIO Mice Inbred C57BL Oxidative Stress Enzyme medicine.anatomical_structure Creatinine biology.protein Anti-Infective Agents Local Cytokines Kidney Diseases Inflammation Mediators Reactive Oxygen Species Oxidation-Reduction Oxidative stress |
| Zdroj: | Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual) Universidade de São Paulo (USP) instacron:USP |
| ISSN: | 1205-7541 |
| Popis: | 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 (WT) or iNOS-deficient (iNOS–/–) mice were treated with ethanol (20% v/v) 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 α in the renal cortex of WT but not iNOS–/– mice. Augmented serum levels of creatinine and increased systolic blood pressure were found in WT 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. |
| Databáze: | OpenAIRE |
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