Incomplete palmitate oxidation in cell-free systems of rat and human muscles

Abstract The palmitate oxidation capacity was determined in whole homogenates, postnuclear fractions and mitochondrial fractions of various rat and human muscles and in rat liver, kidney, brain and lung. The oxidation rate (production of 14 CO 2 and 14 C-labeled acid-soluble intermediates) was [1- 14 C ] palmitate > [ U - 14 C ] palmitate > [16- 14 C ] palmitate in all cell-free systems. Oxidation rates were highest in rat heart and liver, intermediate in kidney, diaphragm and m. quadriceps, and low in brain and lung. The capacity of human heart was much lower than that of rat heart and about twice that of human skeletal muscles. Omission of l -carnitine and addition of malonyl-CoA, KCN or antimycin A decreased the oxidation rates in whole homogenates and mitochondrial fractions. Antimycin or KCN increased and malonyl-CoA decreased the ratio of the oxidation rates with [1- 14 C]- and [16- 14 C]palmitate. The carnitine concentration had no significant effect on the ratio. 14 C-labeled dodecanoic and tetradecanoic acids were identified in homogenates and mitochondrial fractions of m. quadriceps and liver of rat as acid-insoluble intermediates of [16- 14 C]palmitate oxidation in the presence and absence of antimycin A. Their amounts recovered can account for the differences in oxidation rates found with [1- 14 C]- and [16- 14 C]palmitate. The incomplete palmitate oxidation in cell-free systems appears to be mainly caused by an inadequate mitochondrial degradation of peroxisomal oxidation products.