Mitochondria from pea (Pisum sativum L. cotyledons and potato (Solanum
tuberosum L.) tubers exhibited a palmitoyl carnitine-dependent, KCN-s
ensitive stimulation of the oxygen uptake measured in the presence of
0.2 mmol . 1(-1) malate (sparker malate), provided a certain concentra
tion range of palmitoylcarnitine was observed. Above this concentratio
n range, which was dependent on the bovine serum albumin (BSA) concent
ration of the reaction mixture, the mitochondrial oxygen uptake was in
hibited by palmitoylcarnitine. Palmitoylcarnitine (racemate) and palmi
toyl-L-carnitine were equally effective in stimulating/inhibiting mito
chondrial oxygen uptake in the presence of sparker malate. The mitocho
ndrial membrane potential generated in the presence of sparker malate
was partially dissipated by palmitoyl-L-carnitine concentrations stimu
lating the mitochondrial oxygen uptake. The formation of acid-soluble
radioactivity in reaction mixtures provided with [1-C-14]palmitoyl-L-c
arnitine was considerably lower than that expected minimally if the pa
lmitoyl-L-carnitine-stimulated oxygen uptake resulted from palmitoyl-L
-carnitine oxidation sparked by malate. Palmitoylcarnitine concentrati
ons resulting in stimulation of the mitochondrial oxygen uptake in the
presence of sparker malate also led to a stimulation of succinate-cyt
ochrome c reductase activity, as well as to an increase in the measura
ble activities of mitochondrial matrix enzymes, indicating loss of bot
h mitochondrial integrity and mitochondrial enzyme latency in the pres
ence of palmitoylcarnitine. Correspondingly, malate-dependent NADH for
mation 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 w
as affected by palmitoylcarnitine in a similar manner to the oxygen up
take of pea cotyledon and potato tuber mitochondria in the presence of
sparker malate. The results lead to the conclusion that the palmitoyl
carnitine-dependent stimulation of mitochondrial oxygen uptake observe
d in the presence of sparker malate results substantially from an enha
nced malate oxidation due to the detergent effect of palmitoylcarnitin
e on the mitochondrial membranes, rather than from palmitoylcarnitine
beta-oxidation.