Proton leak modulation in testicular mitochondria affects reactive oxygen species production and lipid peroxidation

Mitochondrial proton leak can account for almost 20% of oxygen consumption and it is generally accepted that this process contributes to basal metabolism. In order to clarify the role of basal proton leak in testicular mitochondria, we performed a comparative study with kidney and liver mitochondria...

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Published in:Cell biochemistry and function 2010-04, Vol.28 (3), p.224-231
Main Authors: Rodrigues, Ana Sofia, Lacerda, Beatriz, Moreno, António J. M., Ramalho-Santos, João
Format: Article
Language:English
Subjects:
Animals
Guanosine Diphosphate - metabolism
Hydrogen Peroxide - metabolism
Ion Channels - metabolism
Kidney - cytology
Linoleic Acid - metabolism
Lipid Peroxidation
Male
Membrane Potential, Mitochondrial - physiology
mitochondria
Mitochondria - metabolism
Mitochondria, Liver - metabolism
Mitochondrial Proteins - metabolism
Oxidants - metabolism
Oxidative Phosphorylation
Oxidative Stress
Oxygen Consumption
proton leak
Protons
Rats
Rats, Wistar
Reactive Oxygen Species - metabolism
reproduction
ROS
testis
Testis - cytology
Uncoupling Protein 2
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Summary:Mitochondrial proton leak can account for almost 20% of oxygen consumption and it is generally accepted that this process contributes to basal metabolism. In order to clarify the role of basal proton leak in testicular mitochondria, we performed a comparative study with kidney and liver mitochondrial fractions. Proton leak stimulated by linoleic acid and inhibited by guanosine diphosphate (GDP) was detected, in a manner that was correlated with protein levels for uncoupling protein 2 (UCP2) in the three fractions. Modulation of proton leak had an effect on reactive oxygen species production as well as on lipid peroxidation, and this effect was also tissue‐dependent. However, a possible role for the adenine nucleotide transporter (ANT) in testicular mitochondria proton leak could not be excluded. The modulation of proton leak appears as a possible and attractive target to control oxidative stress with implications for male gametogenesis. Copyright © 2010 John Wiley & Sons, Ltd.
ISSN:0263-6484
1099-0844
DOI:10.1002/cbf.1644