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Nutrition : Mead acid studies
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 Message 68 of 81 in Discussion 
From: MSN Nicknametaka00381  in response to Message 1Sent: 2/4/2008 5:01 AM
The Journal of Nutritional Biochemistry
Volume 3, Issue 11, November 1992, Pages 562-579

Biochemical and nutritional aspects of eicosanoids

Vishwanath M. Sardesai
Wayne State University School of Medicine, Detroit, MI, USA

The eicosanoids are derived from 20-carbon polyunsaturated fatty acids e.g., dihomogamma linolenic, arachidonic, eicosapentaenoic, and Mead acid, which are present as components of cell membrane phospholipids. Activation of phospholipases causes release of these fatty acids that can be metabolized either via the cyclooxygenase pathway to produce the prostanoids—prostaglandins, thromboxanes, and prostacyclins—or via the lipoxygenase pathway to form leukotrienes and lipoxins. These fatty acids can also be oxidized by the cytochrome P-450 system giving rise to several metabolites including epoxyeicosatrienoic acids. Eicosanoids are highly active substances with diverse biological actions. Because arachidonic acid is the most common fatty acid present in tissue lipids, the eicosanoids derived from it predominate in human tissues. Some of the eicosanoids formed from arachidonic acid such as thromboxane A2 and leukotrienes have deleterious effects, while those derived from other polyunsaturated fatty acids are generally less potent or have beneficial actions. The steroidal anti-inflammatory agents, such as cortisone, block the release of precursor fatty acids and thus the formation of all eicosanoids. Non-steroidal anti-inflammatory agents such as aspirin inhibit cyclooxygenase and prevent the production of prostanoids. It is possible to modulate the precursor fatty acid component in cell membrane phospholipids by dietary means, which in turn can alter the types of eicosanoids formed endogenously. Some food constituents such as vitamin C, vitamin E, garlic, onion, ginger, and alcohol can affect the production of eicosanoids. The dietary manipulation may serve as a long-term strategy to favorably modify the endogenous eicosanoid production.