11,12-Epoxyeicosatrienoic acid

From NuGOwiki

The NuGOwiki Metabolite Database is a joint initiative of NuGO and HMDB

Taxonomy Navigation Box; search by

11,12-Epoxyeicosatrienoic acid
2D structure for 11,12-Epoxyeicosatrienoic acid
Chemical Name	(5E,8E)-10-[3-[(E)-oct-2-enyl]oxiran-2-yl]deca-5,8-dienoic acid
Chemical Formula	C₂₀H₃₂O₃
CAS Number	81276-02-0
Chemical Information	HMDB04673
Biochemical Taxonomy	Fatty Acids
Functional Taxonomy	Not Available
Nutritional Taxonomy	Not Available
Metabolic Pathways	Not Available
Biofluid Location	Not Available
Tissue Location	Epidermis
Normal Biofluid Concentrations	Not Available
Normal Tissue Concentrations	Not Available
Diseases / Conditions Related to Nutrition	Not Available
Other (Monogenic Disorders)	Not Available
Abnormal Biofluid Concentrations	Not Available
Abnormal Tissue Concentrations	Not Available
Physiological Processes	Not Available

Authors:
Affiliations:

Introduction

guidelines
11,12-Epoxyeicosatrienoic acid is an epoxyeicosatrienoic acid (EET). Induction of CYP2C8 in native coronary artery endothelial cells by beta-naphthoflavone enhances the formation of 11,12-epoxyeicosatrienoic acid, as well as endothelium-derived hyperpolarizing factor-mediated hyperpolarization and relaxation. Transfection of coronary arteries with CYP2C8 antisense oligonucleotides resulted in decreased levels of CYP2C and attenuated the endothelium-derived hyperpolarizing factor-mediated vascular responses. Thus, a CYP-epoxygenase product is an essential component of the endothelium-derived hyperpolarizing factor-mediated relaxation in the porcine coronary artery, and CYP2C8 fulfills the criteria for the coronary endothelium-derived hyperpolarization factor synthase. The role of EETs in regulation of the cerebral circulation has become more important, since it was realized that EETs are produced in another specialized cell type of the brain, the astrocytes. It has become evident that EETs released from astrocytes may mediate cerebral functional hyperemia. Molecular and pharmacological evidence hve shown that neurotransmitter release and spillover onto astrocytes can generate EETs. Since these EETs may reach the vasculature via astrocyte foot-processes, they have the same potential as their endothelial counterparts to hyperpolarize and dilate cerebral vessels. P450 enzymes contain heme in their catalytic domain and nitric oxide (NO) appears to bind to these heme moieties and block formation of P450 products, including EETs. Thus, there appears to be crosstalk between P450 enzymes and NO/NO synthase. The role of fatty acid metabolites and cerebral blood flow becomes even more complex in light of data demonstrating that cyclooxygenase products can act as substrates for P450 enzymes. (PMID: 17494091, 17468203, 17434916, 17406062, 17361113, 15581597, 11413051, 10519554)