A mutation in succinate dehydrogenase cytochrome b causes oxidative stress and ageing in nematodes

Naoaki Ishii (), Michihiko Fujii, Philip S. Hartman, Michio Tsuda, Kayo Yasuda, Nanami Senoo-Matsuda, Sumino Yanase, Dai Ayusawa and Kenshi Suzuki
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Naoaki Ishii: Tokai University School of Medicine
Michihiko Fujii: Kihara Institute for Biological Research, Yokohama City University
Philip S. Hartman: Texas Christian University
Michio Tsuda: Tokai University School of Medicine
Kayo Yasuda: Tokai University School of Medicine
Nanami Senoo-Matsuda: Tokai University School of Medicine
Sumino Yanase: Tokai University School of Medicine
Dai Ayusawa: Kihara Institute for Biological Research, Yokohama City University
Kenshi Suzuki: Tokai University School of Medicine

Nature, 1998, vol. 394, issue 6694, 694-697

Abstract: Abstract Much attention has focused on the aetiology of oxidative damagein cellular and organismal ageing1,2,3,4. Especially toxic arethe reactive oxygen byproducts of respiration and other biological processes5. A mev-1 (kn1 ) mutant of Caenorhabditis elegans has been found to be hypersensitive to raised oxygen concentrations6,7. Unlike the wild type, its lifespan decreases dramatically as oxygen concentrations are increased from 1 to 60% (ref. 7). Strains bearing this mutation accumulate markers of ageing (such as fluorescent materials and protein carbonyls) faster than the wild type8,9. We show here that mev-1 encodes a subunit of the enzyme succinate dehydrogenase cytochrome b , which is a component of complex II of the mitochondrial electron transport chain. We found that the ability of complex II to catalyse electron transport from succinate to ubiquinone is compromised in mev-1 animals. This may cause an indirect increase in superoxide levels, which in turn leads to oxygen hypersensitivity and premature ageing. Our results indicate that mev-1 governs the rate of ageing by modulating the cellular response to oxidative stress.

Date: 1998
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DOI: 10.1038/29331

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