Mitochondrial Ca2+ fluxes: role of free fatty acids, acyl-CoA and acylcarnitine.
It has been suggested that accumulation of lipid metabolites, such as fatty acids, fatty acyl-CoA and acylcarnitine, in the ischaemic myocardium, may be responsible for disturbances in mitochondrial Ca2+ fluxes. In view of the presence of an intracellular fatty acid binding protein, the question arose whether these intermediates affect mitochondrial Ca2+ uptake and release similarly in vivo. In this study the effects of linoleic acid, palmitic acid, palmitoyl-CoA and palmitoylcarnitine were studied on mitochondrial Ca2+ fluxes in the absence and presence of albumin, an avid binder of fatty acid derivatives. Albumin reversed the effects of the above compounds on mitochondrial Ca2+ uptake and release, suggesting that the presence of an intracellular fatty acid binding protein may protect the ischaemic myocardial cell against the deleterious effects of accumulated fatty acid derivatives.
D000214:Acyl Coenzyme A / Q000494:pharmacology*; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D002331:Carnitine / Q000031:analogs & derivatives*; D007700:Kinetics; D019787:Linoleic Acid; D008041:Linoleic Acids / Q000494:pharmacology*; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects; D019308:Palmitic Acid; D010169:Palmitic Acids / Q000494:pharmacology*; D010171:Palmitoyl Coenzyme A / Q000494:pharmacology*; D010172:Palmitoylcarnitine / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012710:Serum Albumin, Bovine / Q000494:pharmacology
D000214:Acyl Coenzyme A; D008041:Linoleic Acids; D010169:Palmitic Acids; D010171:Palmitoyl Coenzyme A; D010172:Palmitoylcarnitine; D012710:Serum Albumin, Bovine; D019308:Palmitic Acid; D019787:Linoleic Acid; D002331:Carnitine; D002118:Calcium