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 regulation of formation of prostaglandins and arachidonoyl-CoA from arachidonic acid in rabbit kidney medulla microsomes by linoleic acid hydroperoxide. Author: Sakuma S, Usa K, Fujimoto Y. Journal: Prostaglandins Other Lipid Mediat; 2006 May; 79(3-4):271-7. PubMed ID: 16647640. Abstract: Under physiological conditions, small amounts of free arachidonic acid (AA) are released from membrane phospholipids, and cyclooxygenase (COX) and acyl-CoA synthetase (ACS) competitively act on this fatty acid to form prostaglandins (PGs) and arachidonoyl-CoA (AA-CoA). In the present study, we investigated the effects of linoleic acid (LA) and 13-hydroperoxyoctadecadienoic acid (13-HPODE) on the PG and AA-CoA formation from high and low concentrations of AA (60 and 5 microM) in rabbit kidney medulla microsomes. The kidney medulla microsomes were incubated with 60 or 5 microM [(14)C]-AA in 0.1M Tris-HCl buffer (pH 8.0) containing cofactors of COX (reduced glutathione and hydroquinone) and cofactors of ACS (ATP, MgCl(2) and CoA). After incubation, PG (as total PGs), AA-CoA and residual AA were separated by selective extraction using petroleum ether and ethyl acetate. LA (10-50 microM) reduced only PG formation from both 60 and 5 microM AA. 13-HPODE (10-50 microM) also reduced PG formation from 60 and 5 microM AA, but the inhibitory potency was much stronger than that by LA. Furthermore, 13-HPODE had the potential to increase the AA-CoA formation with a decrease in the PG formation from 5 microM AA. These results suggest that 13-HPODE, but not LA, may shift AA away from COX pathway into ACS pathway under low substrate concentration (near physiological concentration of AA).[Abstract] [Full Text] [Related] [New Search]