Little is known about the ability of carnitine to modulate cell functions. As carnitine plays an important role in lipid metabolism we investigated the acute effect of L-carnitine, L-acetyl carnitine and L-propionyl carnithe (300 mg/kg per d; 4 d) on the basal and calcium-ionophore (A23187)-stimulated release of arachidonic acid metabolites from rat carrageenan-elicited peritoneal macrophages. A decrease in the number of peritoneal carrageenan-elicited macrophages was observed after feeding all three compounds. The basal release of prostaglandin E,, 6 keto-prostaglandin F,, and leukotriene B, was stimulated by all treatments. In contrast, thromboxane B, production was diminished by feeding carnitine and acetyl carnitine. A23187-stimulated synthesis of 6 keto-prostaglandin F,, and leukotriene B, was further enhanced by all three compounds. Acetyl carnitine and propionyl carnitine also enhanced thromboxane B, synthesis. However, no effects on prostaglandin E, formation were detected. The 6 keto-prostaglandin Flm: thromboxane B, ratio, calculated from the basal and A23187-stimulated values, was increased by carnitine treatment. In the presence of A231 87 there was also an increase in the 6 keto-prostaglandin F,,:leukotriene B, ratio. We conclude that carnitine, and possibly some of its derivatives, could modify the macrophage component of an inflammation in vivo.Carnitine compounds : Peritoneal macrophages : Arachidonic acid metabolites : Rat L-Carnitine (P-hydroxy-(y-N-trimethy1amino)-butyrate) is a natural amino acid, found particularly in animal cells, which plays an important role in fatty acid (FA) metabolism. Its major function appears to be the transport of long-chain fatty acids into mitochondria for oxidation, particularly in the heart and skeletal muscles. It has also been suggested that under abnormal metabolic conditions, e.g. diabetes, carnitine could act as a buffer for excess organic acids, so protecting mitochondria1 integrity. Its most important medical use is in treating conditions characterized by a carnitine deficiency, resulting from either a genetic defect or medical intervention, e.g. an operation or renal dialysis (Bremer, 1983). It has also been suggested that carnitine supplements may be useful in reversing Intralipid@-induced immunosuppression (De Simone et a/. 1982).Recently carnitine has been shown to modify lipid metabolism in a way which indicates that it could play a more general regulatory role than was previously thought. Specifically, carnitine has been shown to enhance the formation of arachidonic acid (AA) from linoleic acid by isolated hepatocytes (Christopherson & Norseth, 198 1). Cyclooxygenase (CO) and lipoxygenase (LO) metabolites of AA (eicosanoids) are important local modulators of inflammations. In general the CO metabolites are anti-and the LO metabolites proinflammatory, and their effects on a target cell or tissue are often opposing. For example,