Abstract
In order to elucidate the mechanism of dilauryl succinate-induced vitamin E deficiency in vivo in chicks, I conducted experiments to study the effect of the metabolites of dilauryl succinate in chicks on hemolysis and the liver mitochondrial lysis, while neither lauryl alcohol nor succinic acid induced mitochondrial lysis in vitro in chicks. These were monolauryl succinate, lauryl alcohol and succinic acid. Monolauryl succinate induced both hemolysis and mitochondrial lysis at the same concentration as that of monolauryl succinate. At the concentration of 40 times that of monolauryl succinate, lauryl alcohol induced hemolysis but succinic acid did not. Neither alpha-tocopherol, selenium nor combination of both exerted preventive effects on the reactions of monolauryl succinate or lauryl alcohol. Monolauryl succinate-induced mitochondrial lysis was not accompanied by lipid peroxidation. The observations were consistent with those in Tween 20-induced hemolysis and mitochondrial lysis, but not with those in hydrogen peroxide-induced hemolysis or with those in glutathione-induced mitochondrial lysis. It was suggested that dilauryl succinate-induced vitamin E deficiencies in vivo in chicks are mainly due to the surface activity, which is not relevant to peroxide formation, of monolauryl succinate and partly to that of lauryl alcohol.
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