All the catecholamines are derived from tyrosine.

Prostaglandins are important autacoids participating in a myriad of physiologic and pathophysiologic processes. Biosynthesis of prostaglandins and eicosanoids is regulated at several enzymatic steps (1). As shown in Fig. 1, liberation of arachidonic acid from membrane phispholipids upon cell activation is catalyzed by phospholipases. This is a rate limiting step. Once arachidonic acid is liberated, it is metabolized via the cyclooxygenase and lipoxygenase pathways. The enzyme that is responsible for catalysis of arachidonic acid into endoperoxides is prostaglandin endoperoxide synthase (prostaglandin G/H synthase, prostaglandin H synthase or cyclooxygenase). This molecule possesses two enzymic activities: cyclooxygenase which catalyzes the oxygenation of arachidonic acid into prostaglandin G2 (PGG2) and peroxidase converting PGG2 into PGH2 (2). Prostaglandin H synthase is upregulated by peroxides including PGG2 but once PGG2 is converted to PGH2, oxygen radicals that are generated appear to cause irreversible inactivation of the cyclooxygenase activity (3-5). This leads to limited synthesis of PGH2. PGH2 is the common precursor for prostacyclin (PGI2), PGE2, PGF, PGD2 and thromboxane A2 (TXA2). With compromised PGH2 synthesis, production of these biologically active metabolites is consequently self-limited. This enzymatic step, hence, plays a central role in controlling eicosanoid biosynthesis.

Baker RR (1990) The eicosanoids: a historical overview. Clinical Biochemistry 23: 455–458.

Lately, intracellular compartmentalization of eicosanoid–synthetic machinery has emerged as a key component in the regulation of eicosanoid synthesis and functions.


Prostaglandins and Other Eicosanoids | Clinical Gate

Research on the alteration of eicosanoid biosynthesis by dietary linoleate supplementation is reviewed extensively.

Here we will review the current knowledge on the functions of lipid bodies as specialized intracellular sites of compartmentalization of signaling with major roles in eicosanoid formation within cells engaged in inflammatory, infectious and neoplastic process.


term:eicosanoids = include leukotrienes and …

So where do the EFAs come in? Well, the EFAs are the substances out of which the prosatglandins are made. Linoleic and alpha-linolenic acid are the "parents" of all the eicosanoids. Linoleic acid (LA) is converted into gamma-linoleic acid (GLA) in the liver. GLA is then converted to dihomo-gamma-linoleic acid (DGLA), which is then either converted to the series 1 prostaglandins or arachidonic acid (AA). The series 2 prostaglandins are made from AA. The series 3 prostaglandins are made from alpha-linolenic acid (LNA) by the following path: LNA is converted into stearidonic acid (SDA - also known as octadecatetraenoic acid), SDA is converted to eicosatetraenoic acid (ETA), ETA is converted to eicosapentaenoic acid (EPA) and EPA is converted to docosapentanoic acid then docosahexanoic acid (DHA). (DHA also goes "backwards" to become EPA). The series 3 prostaglandins are then made from EPA. EPA blocks both the conversion of DGLA to AA and the conversion of the AA into PGE2 (incidently, so does regular aspirin) and has also been shown to have a significant positive effect on the integrity of muscle cells after exercise stress. Also, high levels of PGE1 prohibit the production of series 2 prostaglandins.

rate limiting step of eicosanoid synthesis

Goetzl EJ, An S and Smith WL (1995) Specificity of expression and effects of eicosanoid mediators in normal physiology and human diseases. FASEB Journal 9: 1051–1058.

Lipid body function in eicosanoid synthesis: An ..

However, it isn't quite as clear-cut as simply labeling the series 2s as "bad". Some series 2 eicosanoids actually counter the "bad" effects of the others series 2s, and so compensate, at least partially, for what would be considered "negative" effects. For instance, prostacyclin PGI2 counters some of the negative effects of prostaglandin PGE2 by inhibiting platelet aggregation and activating leukocytes (which is good). In addition, a couple of the series 2s are potent stimulators of muscle growth. When muscle cells are strenuously trained they release the series 2 prostaglandins PGE2 and PGF2-alpha. PGE2 increases protein degradation, but it also potently induces muscle satellite cell proliferation and infusion, leading to muscle growth. PGF2-alpha increases protein synthesis, suspectedly by increasing protein synthesis "efficiency" at the ribosomes. It also seems to destroy fat cells. (Is that possible support for the theory of "spot reduction" that the old-timers swore by? Train a muscle more often, release more PGF2-alpha, destroy more fat cells?! Incidently, recent research has given scientific support to the concept of "spot reduction".)