Effect of palmitoylcarnitine on mitochondrial activities

Abstract

Mitochondria from pea (Pisum sativum L.) cotyledons and potato (Solanum tuberosum L.) tubers exhibited a palmitoyl carnitine-dependent, KCN-sensitive stimulation of the oxygen uptake measured in the presence of 0.2mmol·−1 malate (sparker malate), provided a certain concentration range of palmitoylcarnitine was observed. Above this concentration range, which was dependent on the bovine serum albumin (BSA) concentration of the reaction mixture, the mitochondrial oxygen uptake was inhibited by palmitoylcarnitine. Palmitoylcarnitine (racemate) and palmitoyl-l-carnitine were equally effective in stimulating/inhibiting mitochondrial oxygen uptake in the presence of sparker malate. The mitochondrial membrane potential generated in the presence of sparker malate was partially dissipated by palmitoyl-lcarnitine concentrations stimulating the mitochondrial oxygen uptake. The formation of acid-soluble radioactivity in reaction mixtures provided with [1-14C]palmitoyll-carnitine was considerably lower than that expected minimally if the palmitoyl-l-carnitine-stimulated oxygen uptake resulted from palmitoyl-l-carnitine oxidation sparked by malate. Palmitoylcarnitine concentrations resulting in stimulation of the mitochondrial oxygen uptake in the presence of sparker malate also led to a stimulation of succinate-cytochrome c reductase activity, as well as to an increase in the measurable activities of mitochondrial matrix enzymes, indicating loss of both mitochondrial integrity and mitochondrial enzyme latency in the presence of palmitoylcarnitine. Correspondingly, malate-dependent NADH formation was stimulated by palmitoylcarnitine. Neither NAD reduction nor oxygen uptake were observed when the mitochondria were provided with palmitoylcarnitine only. The oxygen uptake due to glycine oxidation by mitochondria from green sunflower (Helianthus annuus L.) cotyledons was affected by palmitoylcarnitine in a similar manner to the oxygen uptake of pea cotyledon and potato tuber mitochondria in the presence of sparker malate. The results lead to the conclusion that the palmitoylcarnitine-dependent stimulation of mitochondrial oxygen uptake observed in the presence of sparker malate results substantially from an enhanced malate oxidation due to the detergent effect of palmitoylcarnitine on the mitochondrial membranes, rather than from palmitoylcarnitine β-oxidation.