These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: The effect of palmitoyl-coenzyme A on rat heart and liver mitochondria. Oxygen consumption and palmitoylcarnitine formation.
    Author: Wood JM, Wallick ET, Schwartz A, Chang CH.
    Journal: Biochim Biophys Acta; 1977 Feb 23; 486(2):331-40. PubMed ID: 836862.
    Abstract:
    Rat heart and liver mitochondria, respectively, oxidized palmitoyl-CoA and palmitoylcarnitine optimally at 20-30 and 10-20 nmol substrate/mg. The oxidation of palmitoyl-CoA was accompanied by a lag in State 3 respiration that was proportional to the palmitoyl-CoA concentration. The delay in State 3 rates was more prolonged in liver than in heart at comparable palmitoyl-CoA levels. A similar range of palmitoyl-CoA concentrations produced significant inhibition of respiration in mitochondria oxidizing glutamate-malate. The inhibition was not due to a detergent effect of palmitoyl-CoA since addition of carnitine restored State 3 rates. Electron microscopic examination of mitochondria at low palmitoyl-CoA levels revealed normal ultrastructure. At comparable concentrations of palmitoyl-CoA, formation of palmitoylcarnitine by mitochondria from rat heart and liver followed first-order kinetics. The apparent first-order rate constants decreased with increasing palmitoyl-CoA. These results suggest that substrate inhibition may influence the rate of palmitoyl carnitine formation even at physiological concentrations of palmitoyl-CoA. The apparent first-order rate constant at palmitoyl-CoA levels (12 nmol palmitoyl CoA/mg) optimally oxidized by liver mitochondria, was one-third the value of the apparent rate constant measured in heart mitochondria at the identical substrate level. The prolongation in time to reach equilibrium may acocunt for the relatively greater respiratory sensitivity of liver mitochondria to increasing levels of palmitoyl-CoA.
    [Abstract] [Full Text] [Related] [New Search]