Sakuma S, Fujimoto Y, Okumura M, Nishida H, Yamamoto I, Fujita T
Department of Hygienic Chemistry, Osaka University of Pharmaceutical Sciences, Japan.
Biochem Int. 1992 Jul;27(2):291-9.
The effects of arachidonic acid and arachidonoyl CoA on the catabolism of prostaglandin E2 in a 105000 x g supernatant fraction from rabbit kidney cortex were examined. Arachidonic acid reduced the 15-hydroxy prostaglandin dehydrogenase activity by 50% at 20 microM, while arachidonoyl CoA showed weak inhibition for the enzyme activity (15% at 20 microM). However, arachidonoyl CoA strongly inhibited the prostaglandin delta 13 reductase activity, the concentration required for 50% inhibition being about 3 microM. The dehydrogenase inhibition by arachidonic acid was non-competitive with regard to NAD+ and prostaglandin E2, respectively. Arachidonoyl CoA was also a non-competitive inhibitor for the reductase with regard to NADH and 15-keto prostaglandin E2, respectively. These results suggest that arachidonic acid and arachidonoyl CoA can be important modulating factors in prostaglandin catabolism by the kidney cortex.
研究了花生四烯酸和花生四烯酰辅酶A对兔肾皮质105000×g上清液组分中前列腺素E2分解代谢的影响。花生四烯酸在20μM时使15-羟基前列腺素脱氢酶活性降低50%，而花生四烯酰辅酶A对该酶活性表现出较弱的抑制作用（20μM时为15%）。然而，花生四烯酰辅酶A强烈抑制前列腺素δ13还原酶活性，50%抑制所需浓度约为3μM。花生四烯酸对脱氢酶的抑制作用分别对NAD+和前列腺素E2而言是非竞争性的。花生四烯酰辅酶A对还原酶而言分别对NADH和15-酮基前列腺素E2也是非竞争性抑制剂。这些结果表明，花生四烯酸和花生四烯酰辅酶A可能是肾皮质前列腺素分解代谢中的重要调节因子。
