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

Search MEDLINE/PubMed


  • Title: Regulation of palmitoylcarnitine oxidation in isolated rat liver mitochondria. Role of the redox state of NAD(H).
    Author: Latipää PM, Kärki TT, Hiltunen JK, Hassinen IE.
    Journal: Biochim Biophys Acta; 1986 Feb 12; 875(2):293-300. PubMed ID: 3002483.
    Abstract:
    The redox-mediated regulation of palmitoylcarnitine oxidation was studied in isolated rat liver mitochondria in which the mitochondrial free NADH/NAD+ ratio was controlled by graded concentrations of acetoacetate and ketomalonate in a rotenone and malonate-inhibited system in the presence of ADP. The NADH/NAD+ ratio was buffered kinetically by adjusting the concentrations of the hydrogen acceptor substances and determined by calibrated NAD(P)H fluorometry of the mitochondrial suspension. A two-fold variation in the beta-oxidation rate and a five-fold variation in the free NADH/NAD+ ratio was obtained in the presence of rotenone. A non-linear negative correlation was found between the acetyl-CoA concentration and the beta-oxidation rate and a negative correlation between the long-chain acyl-CoA concentration and the beta-oxidation rate. The data indicate that the redox state is a partial controller of the beta-oxidation rate in liver mitochondria. The contribution of acetyl-CoA, a putative regulator of beta-oxidation at the acyl-CoA thiolase step is small under the conditions used.
    [Abstract] [Full Text] [Related] [New Search]