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Eicosanoid catabolism

Prior to the demonstration of AA metabolism by P450, several groups demonstrated the role of microsomal P450s in the o>/a)-l hydroxylation of prostanoids "- and, more recently, leukotrienes- . Most of these reactions are considered to be involved in eicosanoid catabolism and excretion, but their potential relevance in eicosanoid bioactivation or inactivation, and/or in the control of organ/cell eicosanoid levels has only begun to be explored. We will first discuss the role of P450 in the metabolism of eicosanoids, and then concentrate on the studies of its role in AA metabolism and bioactivation. [Pg.532]

Data in the literature clearly show that CLA seems to positively interfere with hpid metabolism, in particular with n-6 PUFAs for eicosanoid formation, mitochondrial and peroxisomal beta oxidation, energy expenditure and eicosanoid catabolism, and with cholesterol metabolism. Most of these data are confined to experimental models, but human studies, even if scarce (especially long-term trials), suggest that CLA enriched products may have a positive impact on human health, extending the dietary inclusion of dairy products to those patients affected by metabolic syndrome. [Pg.659]

TNF (17.5) Monocyte/macrophage, lymphocyte, neutrophil, endothelium, fibroblast, keratinocyte Activation of T and B cells, natural killer cells, neutrophils, and osteoblasts. Stimulation of endothelial cells to release chemotactic proteins, NO and PGI2. Tumoricidal activity. Induces fever, sleep, hepatic acute phase protein synthesis, catabolism, ACTH release. Lead to myocardial depression, hypotension/shock, hypercoagulability, and death. Stimulates production of IL-1, IL-6, IL-8, IFN-y, and H202. Suppression of cytochrome P-450, thyroglobulin, and lipoprotein lipase. Induces complement activation, release of eicosanoids, including PAF. Procoagulant activity. [Pg.59]

Hyperglycemia followed by hypoglycemia Catabolic hormones release Platelet-activating factor and eicosanoid release... [Pg.319]

Eicosanoids exert specific physiological effects on target cells, like hormones. However, eicosanoids are distinct from most hormones in that they act locally, near their sites of synthesis, and they are catabolized extremely rapidly. Thus, eicosanoids are considered to be locally acting hormones. [Pg.1428]

Pace-Asciak, C. and Smith, W.L. (1983). Enzymes in the biosynthesis and catabolism of the eicosanoids prostaglandins, thromboxanes, leukotrienes, and hydroxy fatty acids. In Boyer, P.D. (ed.) The Enzymes, Vol. 16. pp. 544-604. (New York Academic Press)... [Pg.242]


See other pages where Eicosanoid catabolism is mentioned: [Pg.420]    [Pg.420]    [Pg.301]    [Pg.1927]    [Pg.635]    [Pg.370]    [Pg.602]    [Pg.533]    [Pg.420]    [Pg.291]    [Pg.184]    [Pg.106]    [Pg.382]   
See also in sourсe #XX -- [ Pg.420 ]




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Eicosanoids

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