Abstract

Lipid peroxidation effects of ferric maltol have been compared with those of ferrous sulphate both in lecithin liposomes and in brush border and mitochondrial membranes prepared from rat small intestine. Ferrous sulphate, but not ferric maltol, initiated peroxidation in liposomes as measured by conjugated diene production, but, with 500 microM ascorbic acid present, both caused intense peroxidation which was inhibitable by N2, tocopherol, maltol and ferrous chelators, but not by OH or H2O2 scavengers. The rate of peroxidation increased with ferrous sulphate concentration up to 100 microM but was independent of ferric maltol concentration between 5-500 microM. Material eluted from rat small intestine contained a reducing factor, similar in size to ascorbic acid, capable of generating ferrous ions from ferric maltol and initiating peroxidation. Peroxidation in mitochondrial membranes appeared unaffected by addition of iron whilst that in brush border membranes was detectable only in the presence of iron. At iron concentrations of 100 microM and above ferric maltol produced less liposomal peroxidation than ferrous sulphate. Maltol itself may delay recycling of Fe3+ to Fe2+. Thus ferric maltol could provide a less toxic alternative to ferrous salts in the oral treatment of iron-deficiency.

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