Myocardial H2O2 production in the unanaesthetized rat. Influence of fasting, myocardial load and inhibition of superoxide dismutase and monoamine oxidase.
Myocardial H2O2 production was studied by means of the in vivo administration of aminotriazole (AT), which inactivates the catalase-H2O2 complex compound I. Measurements of the residual catalase activity in male and female rats indicate that beta-oxidation of fatty acids in peroxisomes does not contribute in a substantial way to energy production in response to fasting or to an increased myocardial load, despite previous data on peroxisomes in myocardium. Superoxide dismutase (SOD) inhibition by diethyldithiocarbamate demonstrates that SOD participates in the production of H2O2 in physiological conditions. Such a role was not demonstrated for monoamine oxidase through inhibition by phenelzine.
D000640:Amitrole / Q000494:pharmacology; D000818:Animals; D002374:Catalase / Q000037:antagonists & inhibitors; D004050:Ditiocarb / Q000494:pharmacology*; D005215:Fasting; D005227:Fatty Acids / Q000378:metabolism; D005260:Female; D006861:Hydrogen Peroxide / Q000378:metabolism*; D008297:Male; D008830:Microbodies / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000201:enzymology*; D010624:Phenelzine / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D013482:Superoxide Dismutase / Q000037:antagonists & inhibitors*; D013859:Thiocarbamates / Q000494:pharmacology*
D005227:Fatty Acids; D013859:Thiocarbamates; D004050:Ditiocarb; D006861:Hydrogen Peroxide; D002374:Catalase; D013482:Superoxide Dismutase; D010624:Phenelzine; D000640:Amitrole