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Overview
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Background
17-ODYA is a potent inhibitor of cytochrome P450 fatty acid ω-hydroxylase [1].
ω-hydroxylase is a member of the cytochrome P450 superfamily of enzymes, which are monooxygenases that involved in synthesis of steroids, cholesterol and other lipids. ω-hydroxylase inactivates and degrades leukotriene B4, a potent mediator of inflammation.
In isolated single cells derived from rat portal vein, 17-ODYA (5 μM) inhibited delayed rectifier current (IK(V)) but didn’t influence A-type current (IK(A)). Also, 17-ODYA (5 μM) increased current flow through Ca-sensitive K-channel (BKCa) [2].
In renal cortical microsomes of rats, 17-ODYA inhibited the formation of epoxyeicosatrienoic acids, 20-hydroxyeicosatetraenoic acid and dihydroxyeicosatrienoic acids with IC50 value < 100 nM. 17-ODYA inhibited the omega-hydroxylation of arachidonic acid by 61.3% and increased sodium excretion and urine flow [1]. In rabbit arteries with both endothelium-intact (E+) and endothelium-removal (E-), 17-ODYA increased the efficacy to angiotensin II. Also, 17-ODYA inhibited Ach-relaxation. 17-ODYA improved vasoconstrictor cyclooxygenase-2 metabolites release by inhibition of prostaglandin-ω-hydroxylase [3].[1]. Zou AP, Ma YH, Sui ZH, et al. Effects of 17-octadecynoic acid, a suicide-substrate inhibitor of cytochrome P450 fatty acid omega-hydroxylase, on renal function in rats. J Pharmacol Exp Ther, 1994, 268(1): 474-481.
[2]. Edwards G, Zygmunt PM, Högestätt ED, et al. Effects of cytochrome P450 inhibitors on potassium currents and mechanical activity in rat portal vein. Br J Pharmacol, 1996, 119(4): 691-701.
[3]. Jerez S, Sierra L, de Bruno MP. 17-Octadecynoic acid improves contractile response to angiotensin II by releasing vasocontrictor prostaglandins. Prostaglandins Other Lipid Mediat, 2012, 97(1-2): 36-42.
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