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Mediators of Inflammation
Volume 2 (1993), Issue 7, Pages S57-S62
Research paper

Effects of carnitine and its congeners on eicosanoid discharge from rat cells: implications for release of TNFα

1Department of Pharmacology, Faculty of Medicine, Erasmus University Rotterdam, P.O. Box 1738, Rotterdam 3000 DR, The Netherlands
2Department of Pharmacology, M.B.L., P.O. Box 45, Rijswijk 2280 AA, The Netherlands

Copyright © 1993 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


THE acyl carrier coenzyme A (CoA) is involved in fatty acid metabolism. The carnitine/CoA ratio is of particular importance in regulating the transport of long-chain fatty acids into mitochondria for oxidation. Also CoA has a role in the formation and breakdown of products from both the cyclooxygenase and lipoxygenase pathways of the precursor arachidonic acid. In the present study the effect of 4 days feeding of 300 mg/kg/day of L-carnitine, acetyl Lcarnitine and propionyl L-carnitine on the basal and calcium ionophore (A23187) stimulated release of arachidonic acid metabolites from rat carrageenin elicited peritoneal cells was investigated. There were two series of experiments carried out. In the first, the harvested peritoneal cell population consisted of less than 90% macrophages and additional polymorphonuclear (PMN) leucocytes. The basal release of prostaglandin E2 (PGE2), 6-ketoprostaglandin F (6-keto-PGF) and leukotriene B4 (LTB4) was stimulated by all treatments. The A23187 stimulated release of 6-keto-PGF and LTB4 was increased by all three compounds. The 6-keto-PGF:TxB2 and 6-keto-PGF:LTB4 ratios were increased by carnitine treatment. These results suggested that carnitine could modify the macrophage component of an inflammatory site in vivo. In the second series of experiments the harvested cell population was highly purified (>95% macrophages) and none of the compounds fed to the rats caused a change of either eicosanoid or TNFα formation. Moreover the 6-keto-PGF:TxB2 and 6-keto-PGF:LTB4 ratios were not enhanced by any of the compounds tested. It is conceivable that in the first series the increased ratios 6-keto-PGF:TxB2 and 6-keto-PGF:LTB4 reflected the effect of carnitine or its congeners on PMN leucocytes rather than on macrophages.