Journal
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
Volume 75, Issue 2, Pages 69-74Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.plefa.2006.06.003
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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 eicosapentaenoic acid (EPA) and 15-hydroperoxyeicosapentaenoic acid (15-HPEPE) on the PG and AA-CoA formations from high and low concentrations of AA (60 and 5 mu M) in rabbit kidney medulla microsomes. The kidney medulla microsomes were incubated with 60 or 5 mu M [C-14]-AA in 0.1 M Tris/HCl buffer (pH 8.0) containing cofactors of COX (reduced glutathione and hydroquinone) and cofactors of ACS (ATP, MgCl2 and CoA). After incubation, PG (as total PGs), AA-CoA and residual AA were separated by selective extraction using petroleum ether and ethyl acetate. EPA reduced the PG and AA-CoA formations from both 60 and 5 M AA. In contrast, 15-HPEPE decreased the PG formation without affecting the AA-CoA formation from 60 mu M AA, and increased the AA-CoA formation at the expense of PG formation when 5 mu M AA was used as substrate concentration. The experiments utilizing Fe2+ and an electron spin resonance (ESR) revealed that 15-HPEPE elicits these effects in the form of hydroperoxy adduct. These results suggest that 15-HPEPE, but not EPA, has the potential to shift AA away from COX pathway into ACS pathway at low substrate concentration (close to the physiological concentration of AA). (c) 2006 Elsevier Ltd. All rights reserved.
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