Abstract
When Neurospora crassa 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 N. crassa 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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
