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Batandier 2006 J Bioenerg Biomembr

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Batandier C, Guigas B, Detaille D, El-Mir MY, Fontaine E, Rigoulet M, Leverve XM (2006) The ROS production induced by a reverse-electron flux at respiratory-chain complex 1 is hampered by metformin . J Bioenerg Biomembr 38:33-42.

Β» PMID: 16732470

Batandier C, Guigas B, Detaille D, El-Mir MY, Fontaine E, Rigoulet M, Leverve XM (2006) J Bioenerg Biomembr

Abstract: Mitochondrial reactive oxygen species (ROS) production was investigated in mitochondria extracted from liver of rats treated with or without metformin, a mild inhibitor of respiratory chain complex 1 used in type 2 diabetes. A high rate of ROS production, fully suppressed by rotenone, was evidenced in non-phosphorylating mitochondria in the presence of succinate as a single complex 2 substrate. This ROS production was substantially lowered by metformin pretreatment and by any decrease in membrane potential (Delta Phi(m)), redox potential (NADH/NAD), or phosphate potential, as induced by malonate, 2,4-dinitrophenol, or ATP synthesis, respectively. ROS production in the presence of glutamate-malate plus succinate was lower than in the presence of succinate alone, but higher than in the presence of glutamate-malate. Moreover, while rotenone both increased and decreased ROS production at complex 1 depending on forward (glutamate-malate) or reverse (succinate) electron flux, no ROS overproduction was evidenced in the forward direction with metformin. Therefore, we propose that reverse electron flux through complex 1 is an alternative pathway, which leads to a specific metformin-sensitive ROS production. β€’ Keywords: Metformin, ROS, oxidative phosphorylation, rat liver mitochondria, rotenone, malonate, antimycin, membrane potential β€’ Bioblast editor: Doerrier C β€’ O2k-Network Lab: FR Grenoble Saks VA, FR Grenoble Schlattner U, FR Bordeaux Devin A


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