If the know-how could be produced practical it would modify society and the financial state radically (which may possibly not be a lousy point) – no will need for the immensely wasteful take in-and-toss-away procedure that the existing economic climate is dependent on. Since the prostaglandin and thromboxane metabolites of 20-HETE absence the platelet-stimulating actions to their prostaglandin and thromboxane precursors and considering the fact that the 12-hydroxy and 11-hydroxy metabolites of 20-HETE might also be inactive, these metabolic pathways seem to perform in inactivating 20-HETE with respect to the platelet method. These shortening pathways also are most likely to serve in inactivating 20-HETE, even though the initial item of this shortening pathway, 20-carboxy-HETE, dilates coronary microvessels in the pig coronary heart and thereby could provide to antagonize the vasoconstrictor steps of 20-HETE, at least in this organ and species. Coronary artery endothelial cells isolated from pigs integrate 20-HETE generally into the sn-2 place of phospholipids as a result of a coenzyme A-dependent approach. Cultured easy muscle mass and endothelial cells from mouse brain microvasculature oxidize 20-HETE to its 20-carboxy analog, 20-carboxy- 5Z,8Z,11Z,14Z-eicosatetraenoic acid, then to 18-carboxy-5Z,8Z,10Z,14Z-octadecatetraenoic acid, and then to the even further chain-shortened dicarboxylic acid, 16-carboxy-5Z,8Z,10E-hexadecatrrenoic acid, in a series of Beta oxidation reactions. It is most likely, even though not yet demonstrated, that these mouse and pig 20-HETE metabolizing pathways also arise in individuals.
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