[Alteration of energy-dependent functions of liver mitochondria during the interaction of the carrier of adenine nucleotides with palmitoyl-CoA].
Palmitoyl-CoA, at the concentrations which did cause uncoupling of oxidative phosphorylation, decreased the energy pool of liver mitochondria in presence of oligomycine. Characteristic ability of palmitoyl-CoA to increase the proton transport in mitochondrial membranes was responsible for the deenergizing action.
D000214:Acyl Coenzyme A / Q000494:pharmacology*; D000818:Animals; D005260:Female; D007700:Kinetics; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism*; D000226:Mitochondrial ADP, ATP Translocases / Q000378:metabolism*; D009713:Nucleotidyltransferases / Q000378:metabolism*; D009840:Oligomycins / Q000494:pharmacology; D010085:Oxidative Phosphorylation / Q000187:drug effects; D010171:Palmitoyl Coenzyme A / Q000494:pharmacology*; D051381:Rats; D013367:Submitochondrial Particles / Q000187:drug effects / Q000378:metabolism
D000214:Acyl Coenzyme A; D009840:Oligomycins; D010171:Palmitoyl Coenzyme A; D000226:Mitochondrial ADP, ATP Translocases; D009713:Nucleotidyltransferases
Izmenenie énergozavisimykh funktsiĭ mitokhondriĭ pecheni pri vzaimodeĭstvii perenoschika adeninnukleotidov s pal'mitoil-KoA.