Platelet-activating factor chemical structures

Platelet activating factor can be defined as a phosphoglyceride with potent inflammatory properties as well as many other physiological and pathological attributes. The most prevalent chemical form of this factor can be represented by the structural formula shown in Figure 6-1, where n = 15 0, 17 0, 17 1 (in highest amounts). Its chemical name is 1 -0-alkyl-2-acetyl-in-glycero-3-phosphocholine. 

FIGURE 6-1. Chemical structure of platelet activating factor. 

Figure 3 The chemical structure of a well-known ether lipid, platelet activating factor, showing stereochemistry. Chemical formula and molecular weight (g/mol) are included.

Fig. 2. Chemical stractures of platelet-activating factor (PAF) and structurally related ether-linked glycerolipids possessing biological activities.

In 1979, the chemical structure of PAF was identified as l-alkyl-2-acetyl-sn-gIycero-3-phosphocholine (Fig. 2) (D.J. Hanahan, 1979 M.L. Blank, 1979 J. Benveniste, 1979). The semi-synthetic preparation tested in these initial experiments aggregated platelets at concentrations as low as 10 " M and induced an anti-hypertensive response when as little as 60 ng were administered intravenously to hypertensive or normotensive rats. Threshold concentrations vary by cell type and organism, but PAF can activate human inflammatory cells at concentrations as low as 10 M. PAF induces diverse biological responses (Table 1) and has been implicated as a contributing factor in the pathogenesis of such diverse disease processes as asthma, hypertension, allergies, inflammation, and anaphylaxis. 

Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone.

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