Subcellular fractions of purified cytoplasmic, nonmembrane-bound lipid bodies were prepared from [³H]-arachidonic acid-labeled guinea pig peritoneal macrophages and line 10 hepatocarcinoma cells. These fractions, which contained [³H]-arachidonyl lipids, were shown to be devoid of contaminating cellular membranes by electron microscopy, and to contain prostaglandin endoperoxide (PGH) synthase by postembedding immunogold electron microscopy. These findings support a proposed role for these lipid-rich organelles in the generation of eicosanoids by oxidative metabolism of arachidonate in the cyclooxygenase pathway of inflammatory and neoplastic cells.

Lipid bodies are nonmembrane-bound cytoplasmic inclusions which are prominent in cells engaged in inflammatory responses. Using postembedding immunogold localization with a primary anti-PGH (prostaglandin endoperoxide) synthase monoclonal antibody, PGH synthase was localized by electron microscopy to lipid bodies of two prostaglandin-forming cells: human eosinophils and murine 3T3 fibroblasts. Freshly isolated eosinophils from a hypereosinophilic syndrome donor and peripheral blood eosinophils maintained in coculture with 3T3 fibroblasts and granulocyte-macrophage colony-stimulating factor were studied. In both cell types, lipid bodies were the predominant structures labeled with anti-PGH synthase. Labeling was absent in controls. In both human eosinophils and murine fibroblasts, lipid bodies represent sites of localization of PGH synthase – the rate-limiting initial enzyme in the formation of prostaglandins – and may serve as specific sites of formation of cyclooxygenase-pathway-derived eicosanoids.

Heparin was secreted from HLMCs which were stimulated by anti-IgE, and heparin was recovered by a combination of conservative and synthetic mechanisms in HLMCs after a secretory event.