Abstract

Glycerophospholipids and sphingolipids typical of the myelin sheath have been examined for the formation of thiobarbituric acid reactive materials after attack by hydroxyl free radicals. Thiobarbituric acid (TBA) reactive materials are formed following exposure of phosphatidylcholine (PC), phosphatidylserine (PS) and phosphatidylethanolamine (PE) to hydroxyl radical attack in the order PS > PC > PE while the sphingolipids, sphingomyelin and cerebroside and the sterol cholesterol, did not form TBA reactive materials. Inclusion of cholesterol into PC vesicles reduced the formation of TBA reactive materials on hydroxyl radical attack while with PS there was an increase. In mixed glycerophospholipid systems inclusion of cerebroside reduced formation of TBA reactive materials following hydroxyl radical attack on phosphatidylcholine and phosphatidylserine, but not phosphatidylethanolamine. The findings are discussed in relation to the oxidative damage we have observed in the central nervous system at different stages of chronic relapsing experimental allergic encephalomyelitis [Brett R. and Rumsby M.G. Neurochem. Int. 23, 35–44 (1993)].

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