Induction by carbon tetrachloride of a lipid peroxidation inhibitor (LPI) present in rat liver soluble fraction.
Oral administration of an adequate amount of carbon tetrachloride to rats resulted in an increase in the ability of the soluble fraction to inhibit microsomal NADPH-dependent lipid peroxidation. Aso, feeding of a fat-free, high carbohydrate diet to rats led an increase in the ability of the soluble fraction to prevent lipid peroxidation. Partial purification of the soluble factor inhibiting lipid peroxidation (LPI) by means of polyethylene glycol 6,000 (PEG) fractionation and hydroxylapatite column chromatography indicated that LPI is not glutathion peroxidase.
D000818:Animals; D002251:Carbon Tetrachloride / Q000494:pharmacology*; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D005227:Fatty Acids; D005979:Glutathione Peroxidase / Q000378:metabolism; D050356:Lipid Metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008862:Microsomes, Liver / Q000378:metabolism; D010545:Peroxides / Q000378:metabolism*; D051381:Rats
D004040:Dietary Carbohydrates; D004041:Dietary Fats; D005227:Fatty Acids; D010545:Peroxides; C013584:lipid peroxidation inhibitor; D002251:Carbon Tetrachloride; D005979:Glutathione Peroxidase