Platelet aggregation, vitamin

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.

Early work revealed evidence of enhanced prostaglandin synthesis in platelets of vitamin-E-deficient animals [122], and the vitamin is known to inhibit platelet aggregation both in vivo and in vitro [ 123]. Further studies have shown that vitamin E can suppress TXA2 synthesis and enhance PGI2 formation [124-126]. 

It is also possible that vitamin E can nullify some of the main adverse effects of oestrogen on blood platelets. Administration of ethynyloestradiol to female rats increased lipid synthesis, mainly lanosterol, and thrombin-induced platelet aggregation. Treatment of the rats with a-tocopheryl acetate depressed the enhanced lipid synthesis and aggregation induced by the oestrogen. In vitro, too, platelet aggregation was enhanced by the addition of lanosterol, and this response was almost completely antagonised by preincubation with a-tocopheryl acetate [145]. 

Vitamin E directly scavenges most of the RS and may also upregulate antioxidant enzymes (20), reduces platelet aggregation and adhesion (21,22), and decreases smooth cell proliferation (23), It is considered as the most classical chain breaker antioxidant, The RDA of vitamin E is 10 mg/day,... 

More recent studies have shown that vitamin E also has roles in cell signaling, by inhibition or inactivation of protein kinase C, and in modulation of gene expression, inhibition of cell proliferation, and platelet aggregation. These effects are specific for a-tocopherol and are independent of the antioxidant properties of the vitamin. 

Freedman JE and Keaney JF Jr. (2001) Vitamin E inhibition of platelet aggregation is independent of antioxidant activity. Journal of Nutrition 131,374S-7S. 

Trans-resveratrol (trans-3,5,4 -trihydroxystilbene) is a non-flavonoid polyphenol found in grapes, mulberries, and other food prod-ucts. It is responsible for the antioxidant activity of red wine. Intake of moderate amount of red wine has been found to reduce the risk of cardiovascular diseases. In addition to antioxidant activity, resveratrol could inhibit platelet aggregation, and showed anticancer activity. The phenoxyl radicals of resveratrol produced during oxidation by hydroxyl radicals, one-electron oxidants, and peroxyl radicals showed absorption maximum at 410 nm (Fig. I). Reports indicate that trans-resveratrol is a better radical scavenger than vitamins E and C and its activity is similar to that of the flavonoids epicatechin and quercetin. From the comparison of the spectral and kinetic properties of the transients derived from trans-resveratrol and its analogues, it could be concluded that in the neutral and acidic solutions, the para-hydroxy... 

Williams, J. C., Forster, L. A., Tull, S. P., Wong, M., Bevan, R. J., and Ferns, G. A. (1997) Dietary vitamin E supplementation inhibits thrombin-induced platelet aggregation, but not monocyte adhesiveness, in patients with hypercholesterolaemia. Int J Exp Pathol 78,259-66. 

Renal insufficiency is a risk factor for the toxic effects of the beta-lactams (321,322), including neurotoxic reactions (323), inhibition of platelet aggregation (324), and to some extent interaction with vitamin K-dependent synthesis of coagulation factors (325). 

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