1887

Abstract

When was grown in the presence of chloramphenicol, the oxidation of NAD-linked substrates by isolated mitochondria became largely insensitive to rotenone. It appears that chloramphenicol hindered the biogenesis of a functional rotenone-sensitive NADH-ubiquinone oxidoreductase. The rotenone-resistant pathway was able to donate electrons to both cyanide-sensitive and -resistant oxidases, indicating the operation of a branched system rather than of parallel respiratory chains. Growth of in the presence of chloramphenicol also strongly enhanced the rates of oxidation of exogenous NADH and NADPH. This increased oxidation by mitochondria was largely insensitive to cyanide. The addition of exogenous AMP to isolated mitochondria did not specifically stimulate the electron flux through the alternative oxidase.

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1983-08-01
2021-08-02
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