Rotenone exerts similar stimulatory effects on H2O2 production by isolated brain mitochondria from young-adult and old rats

Autor(es)

Michelini, Luiz G. B. ^[1] ; Figueira, Tiago R. ^[1] ; Siqueira-Santos, Edilerie S. ^[1] ; Castilho, Roger F. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Estadual Campinas, Fac Ciencias Med, Dept Patol Clin, BR-13083887 Campinas, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Neuroscience Letters; v. 589, p. 25-30, MAR 4 2015.
• Citações Web of Science: 4

Resumo

Chronic and systemic treatment of rodents with rotenone, a classical inhibitor of mitochondrial respiratory complex I, results in neurochemical, behavioral, and neuropathological features of Parkinson's disease. The aim of the present study was to evaluate whether brain mitochondria from old rats (24 months old) would be more susceptible to rotenone-induced inhibition of oxygen consumption and increased generation of H2O2 than mitochondria from young-adult rats (3-4 months old). Isolated brain mitochondria were incubated in the presence of different rotenone concentrations (5, 10, and 100 nM), and oxygen consumption and H2O2 production were measured during respiratory states 3 (ADP-stimulated respiration) and 4 (resting respiration). Respiratory state 3 and citrate synthase activity were significantly lower in mitochondria from old rats. Mitochondria from young-adult and old rats showed similar sensitivity to rotenone-induced inhibition of oxygen consumption. Similarly, H2O2 production rates by both types of mitochondria were dose-dependently stimulated to the same extent by increasing concentrations of rotenone. We conclude that rotenone exerts similar effects on oxygen consumption and H2O2 production by isolated brain mitochondria from young-adult and old rats. Therefore, aging does not increase the mitochondrial H2O2 generation in response to complex I inhibition. (C) 2015 Elsevier Ireland Ltd. All rights reserved. (AU)

• Processo FAPESP: 11/50400-0 - Metabolismo energético, estado redox e funcionalidade mitocondrial na morte celular e em desordens cardiometabólicas e neurodegenerativas
• Beneficiário: Aníbal Eugênio Vercesi
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 11/51800-1 - Dano muscular induzido por exercício excêntrico: envolvimento da mitocôndria e interações com a miotoxicidade da estatina
• Beneficiário: Tiago Rezende Figueira
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 11/14229-4 - Produção mitocondrial de espécies reativas de oxigênio na presença de inibição parcial do complexo I: Efeito de diferentes estados metabólicos
• Beneficiário: Luiz Guilherme Michelini Bueno
• Modalidade de apoio: Bolsas no Brasil - Mestrado