Prostaglandin H2

From NuGOwiki

(Redirected from HMDB01381)

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

Taxonomy Navigation Box; search by

Prostaglandin H2
2D structure for Prostaglandin H2
Chemical Name	7-[5-(3-hydroxyoct-1-enyl)-2,3-dioxabicyclo[2.2.1]hept-6-yl]hept-5-enoic acid
Chemical Formula	C₂₀H₃₂O₅
CAS Number	42935-17-1
Chemical Information	HMDB01381
Biochemical Taxonomy	Prostanoids
Functional Taxonomy	Not Available
Nutritional Taxonomy	Not Available
Metabolic Pathways	Not Available
Biofluid Location	Not Available
Tissue Location	Platelet
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
Prostaglandin H2 (PGH2) is the first intermediate in the biosynthesis of all prostaglandins. Prostaglandins are synthesized from arachidonic acid by the enzyme COX-1 and COX-2, which are also called PGH synthase 1 and 2. These enzymes generate a reactive intermediate PGH2 which has a reasonably long half-life (90-100 s) but is highly lipophilic. PGH2 is converted into the biologically active prostaglandins by prostaglandin isomerases, yielding PGE2, PGD2, and PGF2, or by thromboxane synthase to make TxA2 or by prostacyclin synthase to make PGI2. Most nonsteroidal anti-inflammatory drugs such as aspirin and indomethacin inhibit both PGH synthase 1 and 2. A key feature for eicosanoid transcellular biosynthesis is the export of PGH2 or LTA4 from the donor cell as well as the uptake of these reactive intermediates by the acceptor cell. Very little is known about either process despite the demonstrated importance of both events. In cells, PGH2 rearranges nonenzymatically to LGs even in the presence of enzymes that use PGH2 as a substrate. When platelets form Thromboxane A2 (TXA2) from endogenous arachidonic acid (AA), PGH2 reaches concentrations very similar to those of TXA2 and high enough to produce strong platelet activation. Therefore, platelet activation by TXA2 appears to go along with an activation by PGH2. The agonism of PGH2 is limited by the formation of inhibitory prostaglandins, especially PGD2 at higher concentrations. That is why thromboxane synthase inhibitors in PRP and at a physiological HSA concentration do not augment platelet activation. (PMID: 2798452, 15650407, 16968946)