Effects of ferrous chloride and iron dextran on lipid peroxidation in vivo in vitamin E and selenium adequate and deficient rats.

The effects of intraperitoneally injected ferrous chloride and iron-dextran on lipid peroxidation in vivo were assessed. Peroxidation was estimated by measuring ethane, a volatile autoxidation product of omega-3-unsaturated fatty acids. Rats supplemented with 0.1 ppm dietary selenium and rats supplemented with 0.1 ppm selenium and 200 IU vitamin E/kg diet were injected with ferrous chloride at 30 mg iron/kg, or with sodium chloride, or left uninjected. In both dietary groups ferrous chloride increased ethane production while sodium chloride did not, but the iron-caused ethane increase was 8 times greater in the low E group. Iron-dextran injected at 500 mg iron/kg was fatal to rats fed a basal diet deficient in selenium and vitamin E or diet supplemented with 0.5 ppm selenium; supplemental vitamin E at 200 IU/kg diet prevented this mortality. Iron-dextran quadrupled ethane production in rats fed the basal diet and tripled ethane production in rats fed the selenium-supplement diet. Vitamin E supplementation prevented the iron-dextran-caused rise in ethane production. A histological examination of rats killed by iron-dextran showed severe generalized necrosis of the diaphragm and severe focal necrosis of thigh muscle. Vitamin E protected more effectively than selenium against iron-dextran-caused peroxidation as well as against acute iron-dextran-caused mortality.