EFFECTS OF IRON, RIBOFLAVIN AND IODIDE DEFICIENCIES ON HEPATIC DRUG-METABOLIZING ENZYME SYSTEMS

¹ Departments of Pediatrics and Biochemical Pharmacology, State University of New York, Buffalo, New York

The effects of three specific nutritional deficiencies (iron, riboflavin and iodide) on hepatic drug-oxidizing, -reducing and -glucuronidating systems, microsomal cytochromes and hexobarbital sleeping times were investigated in adult Swiss-Webster mice. Chronic iron deficiency resulted in statistically significant increases in hexobarbital side chain oxidation, aminopyrine N-demethylation and microsomal cytochrome b₅ concentrations, but no significant change occurred in sleeping times and in cytochrome P-450 content. Riboflavin deficiency in weanling mice resulted in a biphasic effect on sleeping times showing an initial decrease followed by an increase after 15 days on the deficient diet. Microsomal cytochrome P-450 content was markedly increased but oxidative metabolisms measured in vitro were augmented only slightly. Iodide deficiency in hypothyroid (propylthiouracil-treated) mice resulted in marked increases in drug-oxidizing activity in vitro, when compared to activities measured in liver homogenates from iodidesupplemented hypothyroid animals. Microsomal content of cytochromes b₅ and P-450 were also increased but p-nitrobenzoic acid reduction and p-nitrophenol conjugation were not affected. Hexobarbital sleeping times correlated well with in vitro enzymic activities in experiments with iodide-deficient mice but little or no correlation was observed in riboflavin-or iron-deficient animals.

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