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Platelet fatty acid metabolism

On the other hand, the increased GPx activity (possibly via protein synthesis) might be associated with an oxidative stress induced by DHA (22 6, endogenous pool in the course of the DHA (22 6, -3) estoified to tri ycerides is rapidly redistributed within blood lipxqnioteins. The DHA (22 6, w-6) bound and circulate with the albumin fraction not only inhibit platelet aggregation but also influences its uptake into phospholipid species by target tissues (98). DHA therefore seems to impact platelet fatty acid metabolism through unique and novel mechanisms. [Pg.283]

Yao JK. Red blood cell and platelet fatty acid metabolism in schizophrenia. In Peet M, Glen I, Horrobin DF, eds. Phospholipid Spectrum Disorder in Psychiatry. Marius, Carnforth, UK. 1999, pp. 57-71. [Pg.344]

Certain bioflavonoids may play a preventive role against cardiovascular diseases. Some citrus and other bioflavonoids have been demonstrated to reduce serum cholesterol levels and to affect fatty acid metabolism (70,71,72). The strong antiadhesive action on red cells and platelets of highly methoxylated flavones such as nobiletin, which also demonstrates antithrombogenic activity (73), indicates an important role in blood rheology and tissue perfusion. The antiadhesive action may indicate a preventive role in atherosclerosis since there is evidence that reduced perfusion of the vascular wall may interact with serum lipids to promote atherogenesis (74). [Pg.52]

Pathways of fatty acid metabolism in human platelets. [Pg.114]

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. 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.
Srivastava, . C. and N. Malhotra. 1991. Acetyl eugenol, a component of oil of cloves (Syzygium aromaticum L.) inhibits aggregation and alters arachidonic acid metabolism in human blood platelets. Prostaglandins Leukot. Essent. Fatty Acid 42 73-81. [Pg.326]

The fatty acid, s )ecifically AA (20 4, functional role in platelet-mediated hemostasis and thrombosis because of its rapid conversion to TxAj upon platelet activation. Over the last few years, we have seen a tremendous interest on AA metabolism within the scientific community. Certainly the interest on PUFAs, has... [Pg.270]

Huzoor-Akbar, Anwer, K., Wince, L. and Kundu, N. Platelet phospholipid metabolism and fatty acid... [Pg.456]

Srivastava KC, Tyagi OD. Effects of a garlic-derived principle (ajoene) on aggregation and arachidonic acid metabolism in human blood platelets. Prostagland Leukotr Essent Fatty Acids 1993 49 587-595. [Pg.144]

Recently Liu and Weller [84] have reviewed the arachidonic acid metabolism in filarial parasites and other helminths. Arachidonic acid (AA) is a 20 carbon polyunsaturated fatty acid derived from dietary fatty acids. In human tissues, AA is usually present in the esterified form such as glycerolipids, phospholipids and neutral lipids. The free AA, released by phospholipases, undergoes various enzymatic oxygenations to form local mediators such as prostaglandins and leukotrienes, which are collectively known as eicosanoids (Chart 9). These eicosanoids are associated with platelet aggregation, vasodilation, leukocyte inflammatory and immune functions and cellular adhesion [85]. [Pg.65]

Linoleic acid and LNA and their long-chain derivatives arc important components of animal and plant cell membranes. When humans ingest fish or fish oil, the EPA and DHA from the diet partially replace the omega-6 fatty acids, especially AA, in the membranes of probably all cells, but especially in the membranes of platelets, erythrocytes, neutrophils, monocytes, and liver cells [reviewed in Simopoulos, 19911. A diet that has a high ratio of omega-6 omega-3 fatty acids has detrimental effects on eicosanoid metabolism and gene expression. [Pg.11]


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See also in sourсe #XX -- [ Pg.112 ]




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