Although the biochemistry and pharmacology of the products of arachidonic acid (AA) oxidation have been described in detail (Samuelsson et al., 1975; Moncada and Vane, 1978; Samuelsson, 1983), questions remain about the early events leading to the formation of these molecules and particularly the sites within the cell from which AA can be initially mobilized. For example, it is widely held that phospho-lipids of cell membranes represent the major source of AA entering the cyclo-oxygenase or lipoxygenase pathways of oxidation. However, alternative routes of AA oxidation have been proposed. Thus, rabbits fed diets deficient in essential fatty acids exhibited markedly diminished content of PGE1, PGE2, and PGF2α in several different organs despite maintaining stable or even supranormal levels of AA and dihomo-γ-linoleic acid in liver or red blood cell membrane phospholipids (Willis et al., 1981). This result suggested that some prostaglandins (“basal pros-taglandins”) may be derived from a metabolic pool of precursors distinct from cellular membranes, although the localization of this metabolic pool within the cell has not been defined (Crawford, 1983).
KeywordsMast Cell Lipid Body Cytoplasmic Granule Human Mast Cell Mouse Peritoneal Macrophage
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