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The ROS Production Induced by a Reverse-Electron Flux at Respiratory-Chain Complex 1 is Hampered by Metformin

Batandier, Cécile, Guigas, Bruno, Detaille, Dominique, El-Mir, M., Fontaine, Eric, Rigoulet, M., Leverve, X. M.·2006·Journal of Bioenergetics and Biomembranes
DOI 10.1007/s10863-006-9003-8
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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.

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Metadata

Authors
Batandier, C., Guigas, B., Detaille, D., El-Mir, M., Fontaine, E., Rigoulet, M., & Leverve, X. M.
Venue
Journal of Bioenergetics and Biomembranes
Publisher
Springer Science and Business Media LLC
Published
2006-02
Volume
38
Issue
1
Pages
33-42
ISSN
  • 0145-479X
  • 1573-6881
DOI
10.1007/s10863-006-9003-8
Cited by
279
References
7
Language
en
Licence
www.springer.com/tdm (tdm)

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