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J. Biochem, 1983, Vol. 94, No. 1 87-96
© 1983 Japanese Biochemical Society

research-article

Detrimental Effects of Methyl Hydroperoxy-Epoxy-Octadecenoate on Mitochondrial Respiration: Detoxication by Rat Liver Mitochondria1

Toshiaki IMAGAWA*, Sabu KASAI**, Kunio MATSUI** and Takao NAKAMURA*

*Department of Molecular Physiology, National Cardiovascular Center Research Institute Suita, Osaka 565
**Division of Biology, Research Institute for Atomic Energy, Osaka City University Sumiyoshi-ku, Osaka, Osaka 556

1. Methyl hydroperoxy-epoxy-octadecenoate (ML-X) inhibited state 3 respiration of rat heart and liver mitochondria with glutamate and malate as substrates. It also inhibited the NADH oxidase and NADH-ubiquinone-1 reductase activities of rat heart and liver submitochondrial particles (SMP).

2. In liver mitochondria and SMP, these inhibitory effects of ML-X were transient, whereas in heart mitochondria and SMP, recovery of the respiratory activities did not occur.

3. Results from high pressure liquid chromatography and 13C-NMR studies indicated that ML-X was converted to hydroperoxy-epoxy-octadecenoic acid (L-X) by incubation with liver mitochondria or SMP but not with heart mitochondria.

4. Purified L-X apparently inhibited state 3 respiration of heart and liver mitochondria with glutamate and malate as substrates, but the amount required for 50% inhibition was 2–3 times larger than that of ML-X.

5. Heart mitochondria adsorbed 36% of the added ML-X, while only 10% of the added L-X was adsorbed.

6. These findings suggest that the recovery of the ML-X-inhibited respiratory activities of liver mitochondria and SMP occurs by conversion of ML-X to L-X, which is only weakly adsorbable on the mitochondrial membrane.

1 This study was supported in part by a Research Grant for Cardiovascular Diseases (56-A) from the Ministry of Health and Welfare.


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