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16(R)-HETE

(Synonyms: 16(R)-Hydroxyeicosatetraenoic Acid) 目录号 : GC40453

A potent vasodilator

16(R)-HETE Chemical Structure

Cas No.:183509-22-0

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产品描述

Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. 16-HETE is a minor CYP450 metabolite of arachidonic acid released by the kidney upon angiotensin II stimulation that demonstrates stereospecific biological activity. Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. 16-HETE is a minor CYP450 metabolite of arachidonic acid released by the kidney upon angiotensin II stimulation that demonstrates stereospecific biological activity. 16(S)-HETE inhibits proximal tubule ATPase activity by as much as 60% at a concentration of 2 µM.[1]

Reference:
[1]. Carroll, M.A., Balazy, M., Margiotta, P., et al. Cytochrome P-450-d]ependent HETEs: Profile of biological activity and stimulation by vasoactive peptides. American Journal of Physiology 271, R863-R869 (1996).

Chemical Properties

Cas No. 183509-22-0 SDF
别名 16(R)-Hydroxyeicosatetraenoic Acid
化学名 16R-hydroxy-5Z,8Z,11Z,14Z-eicosatetraenoic acid
Canonical SMILES CCCCC(O)/C=C\C/C=C\C/C=C\C/C=C\CCCC(=O)O
分子式 C20H32O3 分子量 320.5
溶解度 0.1 M Na2CO3: 2 mg/ml,DMF: Miscible,DMSO: Miscible,Ethanol: Miscible,PBS (pH 7.2): 0.8 mg/ml 储存条件 Store at -20°C
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1 mM 3.1201 mL 15.6006 mL 31.2012 mL
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10 mM 0.312 mL 1.5601 mL 3.1201 mL
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Research Update

16(R)-hydroxy-5,8,11,14-eicosatetraenoic acid, a new arachidonate metabolite in human polymorphonuclear leukocytes

Biochem Pharmacol 2000 Aug 1;60(3):447-55.PMID:10856441DOI:10.1016/s0006-2952(00)00345-2.

Intact human polymorphonuclear leukocytes (PMNL) incubated with substimulatory amounts of arachidonic acid in the absence of a calcium ionophore formed four metabolites that were isolated by reverse-phase HPLC and characterized structurally by GC/MS. A major metabolite eluting as the most abundant peak of radioactivity lacked UV chromophores above 215 nm, and its formation was sensitive to 2-diethylaminoethyl-2,2-diphenylvalerate hydrochloride (SKF525A) but not 3-amino-1-[m(trifluoromethyl)phenyl]-2-pyrazoline (BW755C), suggesting that it was likely to be a product of cytochrome P450. The GC/MS analysis revealed the presence of two components: 20-hydroxy-5,8,11,14-eicosatetraenoic acid (20-HETE) and 16-hydroxy-5,8,11,14-eicosatetraenoic acid (16-HETE) in an approximate ratio of 4:1. The minor metabolites were identified as 15-HETE and 5-HETE. Although 20-HETE has been observed previously as a product of arachidonic acid metabolism in PMNL, the occurrence of 16-HETE was a novel finding. The stereochemistry of the hydroxyl group in PMNL-derived 16-HETE was established by analysis of 1-pentafluorobenzyl-16-naphthoyl derivatives on a chiral-phase chromatographic column and comparison with authentic synthetic stereoisomers. The PMNL-derived radioactive metabolite co-eluted with the synthetic 16(R)-HETE stereoisomer. Analysis of the total lipid extracts from intact PMNL followed by mild alkaline hydrolysis resulted in detectable amounts of 16-HETE (108+/-26 pg/10(8) cells) and 20-HETE (341+/-69 pg/10(8) cells), which suggested that these HETEs were formed from endogenous arachidonic acid and esterified within PMNL lipids. Thus, in contrast to calcium ionophore-stimulated neutrophils that generate large amounts of 5-lipoxygenase products, the intact PMNL generate 20-HETE and 16(R)-HETE via a cytochrome P450 omega- and omega-4 oxygenase(s).

16(R)-hydroxyeicosatetraenoic acid, a novel cytochrome P450 product of arachidonic acid, suppresses activation of human polymorphonuclear leukocyte and reduces intracranial pressure in a rabbit model of thromboembolic stroke

Neurosurgery 2000 Dec;47(6):1410-8; discussion 1418-9.PMID:11126912doi

Objective: Activated polymorphonuclear leukocytes (PMNs) have been suggested to contribute to the development of increased intracranial pressure (ICP). We recently demonstrated that human PMNs produce a novel cytochrome P450-derived arachidonic acid metabolite, 1 6(R)-hydroxyeicosatetraenoic acid [16(R)-HETE], that modulates their function. It was thus of interest to examine this novel mediator in an acute stroke model. Methods: 16-HETE was assessed initially in a variety of human PMN and platelet in vitro assays and subsequently in an established rabbit model of thromboembolic stroke. A total of 50 rabbits completed a randomized, blinded, four-arm study, receiving 16(R)-HETE, tissue plasminogen activator, both, or neither. Experiments were completed 7 hours after autologous clot embolization. The primary end point for efficacy was the suppression of increased ICP. Results: In in vitro assays, 16(R)-HETE selectively inhibited human PMN adhesion and aggregation and leukotriene B4 synthesis. In the thromboembolic stroke model, animals that received 16(R)-HETE demonstrated significant suppression of increased ICP (7.7 +/- 1.2 to 13.1 +/- 2.7 mm Hg, baseline versus final 7-h time point, mean +/- standard error), compared with either the vehicle-treated group (7.7 +/- 0.9 to 15.8 +/- 2.6 mm Hg) or the tissue plasminogen activator-treated group (7.6 +/- 0.6 to 13.7 +/- 2.1 mm Hg). The group that received the combination of 16(R)-HETE plus tissue plasminogen activator demonstrated no significant change in ICP for the duration of the protocol (8.6 +/- 0.6 to 11.1 +/- 1.2 mm Hg). Conclusion: 16(R)-HETE suppresses the development of increased ICP in a rabbit model of thromboembolic stroke and may serve as a novel therapeutic strategy in ischemic and inflammatory pathophysiological states.

Enantioselective substrate specificity of 15-lipoxygenase 1

Biochemistry 2004 Dec 21;43(50):15720-8.PMID:15595827DOI:10.1021/bi048312s.

15-Lipoxygenases are lipid-peroxidizing enzymes which have been implicated in the pathogenesis of various diseases, such as inflammation, atherosclerosis, and osteoporosis. Although the crystal structures for several lipoxygenase isoforms have been solved, there is little information on the substrate alignment at the active site and its impact on the catalytic mechanism. Investigating the oxygenation of specifically designed hydroxy fatty acids, we observed a pronounced enantioselectivity of 15-lipoxygenases for substrates carrying the oxygen moiety in close proximity to the site of hydrogen abstraction [16(R/S)-HETE, 17(R/S)-HETE]. To investigate the mechanistic basis for this unexpected behavior, we applied a strategy involving targeted substrate modification, site-directed mutagenesis, and structural modeling of the enzyme-substrate complex. Taken together, our data suggest that an (S)-hydroxy group in 16-HETE may form a hydrogen bridge between the substrate molecule and Gln548, which contributes to proper alignment of the fatty acid derivative at the active site of the enzyme. This interaction, which was not observed with 16(R)-HETE, 18(R)-HETE, or 18(S)-HETE, appears to be a major reason for the high degree of enantioselectivity during lipoxygenation of 16-HETE.

Study on the levels of N-nitrosamine compounds and untargeted metabolomics in patients with colorectal cancer

Anal Bioanal Chem 2022 May;414(11):3483-3496.PMID:35174409DOI:10.1007/s00216-022-03969-w.

Plasma samples were collected from 34 patients with advanced CRC and 92 healthy persons (control group), and the levels of 9 VNAs were measured using GC-MS. Untargeted metabolomics analysis was performed using LC-MS/MS. Partial least squares discriminant analysis (PLS-DA) and hierarchical cluster analysis were used to determine differential metabolites between the 2 groups. Receiver operating characteristic (ROC) curve analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis were performed on the differential metabolites. It turned out that the detection rates of N-nitrosodimethylamine (NDMA) and N-nitrosopyrrolidine (NPYR) in patients with CRC were higher than in the control group (P < 0.05). N-nitrosomethylethylamine (NMEA) and N-nitrosodiphenylamine (NDPhA) were not detected in CRC patients. NDMA, N-nitrosodibutylamine (NDBA), N-nitrosopiperidine (NPIP), and NPYR were detected in male and female patients with CRC. There was no difference in VNAs exposure between the sexes of CRC patients. In the positive and negative ion mode, a total of 132 differential metabolites and 6 differential metabolic pathways were detected. Adenosine 5'-monophosphate, hypoxanthine, 11,12-epoxy-(5Z,8Z,11Z)-icosatrienoic acid, 16(R)-HETE, acetylcarnitine, and lysophosphatidic acid (LPA 20:5, LPA 20:4) were candidate biomarkers with higher predictive value. Hypoxanthine and xanthine metabolic pathways were associated with changes in VNAs in CRC patients. In summary, the effects of changes of VNAs in the plasma of CRC patients (especially NDMA and NPYR) on the progression of CRC should attract attention. Abnormalities of adenine and guanine and downstream hypoxanthine-xanthine metabolic pathways were closely related to changes of VNAs and metabolomics in CRC patients.

Significant Improvement Selected Mediators of Inflammation in Phenotypes of Women with PCOS after Reduction and Low GI Diet

Mediators Inflamm 2017;2017:5489523.PMID:28655971DOI:10.1155/2017/5489523.

Many researchers suggest an increased risk of atherosclerosis in women with polycystic ovary syndrome. In the available literature, there are no studies on the mediators of inflammation in women with PCOS, especially after dietary intervention. Eicosanoids (HETE and HODE) were compared between the biochemical phenotypes of women with PCOS (normal and high androgens) and after the 3-month reduction diet. Eicosanoid profiles (9(S)-HODE, 13(S)-HODE, 5(S)-HETE, 12(S)-HETE, 15(S)-HETE, 5(S)-oxoETE, 16(R)-HETE, 16(S)-HETE and 5(S), 6(R)-lipoxin A4, 5(S), 6(R), 15(R)-lipoxin A4) were extracted from 0.5 ml of plasma using solid-phase extraction RP-18 SPE columns. The HPLC separations were performed on a 1260 liquid chromatograph. No significant differences were found in the concentration of analysed eicosanoids in phenotypes of women with PCOS. These women, however, have significantly lower concentration of inflammatory mediators than potentially healthy women from the control group. Dietary intervention leads to a significant (p < 0.01) increase in the synthesis of proinflammatory mediators, reaching similar levels as in the control group. The development of inflammatory reaction in both phenotypes of women with PCOS is similar. The pathways for synthesis of proinflammatory mediators in women with PCOS are dormant, but can be stimulated through a reduction diet. Three-month period of lifestyle change may be too short to stimulate the pathways inhibiting inflammatory process.