Acyl-carnitine effects on isolated cardiac mitochondria and erythrocytes.
The effects of various long-chain acyl-carnitines (AC) on mitochondrial functions and red cell membrane stability were studied. Lower concentrations slightly stimulate respiration-dependent functions such as phosphorylation rate and Ca++ uptake velocity, whereas higher concentrations inhibit these functions with concomitant depression of the ATP/O ratio. The order of effectiveness among the AC is very similar for different mitochondrial functions. The differences among AC in their actions on red cell stability in hypotonic media and their differences in influence on mitochondrial functions exhibit less resemblance. The relative order of erythrolytic concentrations of AC follows the order of their critical micellar concentrations. Model calculations indicate that the concentrations of AC found in ischemic hearts are below those which exhibit inhibitory effects in vitro. Ultrastructural changes in mitochondria incubated with AC are different from those found in ischemic tissue. From this, it seems questionable whether the elevated AC levels in ischemic hearts are indeed as important for the development of membrane damage as is often supposed.
D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002331:Carnitine / Q000031:analogs & derivatives* / Q000494:pharmacology; D004910:Erythrocyte Membrane / Q000502:physiology*; D006168:Guinea Pigs; D008823:Micelles; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D009206:Myocardium / Q000473:pathology; D009996:Osmotic Fragility / Q000187:drug effects*; D010085:Oxidative Phosphorylation; D010101:Oxygen Consumption
D008823:Micelles; D000255:Adenosine Triphosphate; D002331:Carnitine; D002118:Calcium