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: Contribution of peroxisomal beta-oxidation system to the chain-shortening of N-(alpha-methylbenzyl)azelaamic acid in rat liver.
    Author: Suzuki H, Mori K, Yamada J, Suga T.
    Journal: Biochem Pharmacol; 1990 Jun 15; 39(12):1975-81. PubMed ID: 2353938.
    Abstract:
    Hepaptic peroxisomal and mitochondrial beta-oxidation of N-(alpha-methylbenzyl)azelaamic acid (C9), which is a possible metabolic intermediate of Melinamide, a potent hypocholesterolemic drug, were investigated. Isolated hepatocytes generated H2O2 when incubated with C9, indicating that C9 served as the substrate for peroxisomal beta-oxidation. Also with isolated peroxisomes a significant activity of peroxisomal beta-oxidation for C9-CoA measured by following cyanide-insensitive NAD reduction was observed, when the chain-shortened products such as C7 and C5 were detected from the incubation mixture of C9-CoA, and so NADH, acetyl-CoA and C2 units split off from C9-CoA were produced in stoichiometric amounts. In contrast, the mitochondrial beta-oxidation for C9 measured by following ketone body production and antimycin A-sensitive O2 consumption was not detectable, indicating that C9 is not metabolized by mitochondrial beta-oxidation. Comparative study of beta-oxidation capacities in peroxisomes and mitochondria indicate that the beta-oxidation of C9 occurs exclusively in peroxisomes. Also, the formation activity of C2 units liberated from C9 in intact hepatocytes reflects the peroxisomal beta-oxidation activity of liver homogenates with a highly close correlation. Therefore, it is concluded that C9 can be an excellent substrate for estimating peroxisomal beta-oxidation activity in intact cells.
    [Abstract] [Full Text] [Related] [New Search]