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Inhibition of Riboflavin Metabolism in Rat Tissues by Chlorpromazine, Imipramine, and Amitriptyline

核黄素 氯丙嗪 三环 丙咪嗪 阿米替林 化学 药理学 黄素单核苷酸 黄素腺嘌呤二核苷酸 利血平 生物化学 硫胺素 辅因子 新陈代谢 医学 替代医学 病理
作者
John T. Pinto,Yee Ping Huang,Richard S. Rivlin
出处
期刊:Journal of Clinical Investigation [American Society for Clinical Investigation]
卷期号:67 (5): 1500-1506 被引量:54
标识
DOI:10.1172/jci110180
摘要

Prompted by recognition of the similar structures of riboflavin (vitamin B(2)), phenothiazine drugs, and tricyclic antidepressants, our studies sought to determine effects of drugs of these two types upon the conversion of riboflavin into its active coenzyme derivative, flavin adenine dinucleotide (FAD) in rat tissues. Chlorpromazine, a phenothiazine derivative, and imipramine and amitriptyline, both tricyclic antidepressants, each inhibited the incorporation of [(14)C]riboflavin into [(14)C]FAD in liver, cerebrum, cerebellum, and heart. A variety of psychoactive drugs structurally unrelated to riboflavin were ineffective. Chlorpromazine, imipramine, and amitriptyline in vitro inhibited hepatic flavokinase, the first of two enzymes in the conversion of riboflavin to FAD. Evidence was obtained that chlorpromazine administration for a 3- or 7-wk period at doses comparable on a weight basis to those used clinically has significant effects upon riboflavin metabolism in the animal as a whole: (a) the activity coefficient of erythrocyte glutathione reductase, an FAD-containing enzyme used as an index of riboflavin status physiologically, was elevated, a finding compatible with a deficiency state, (b) the urinary excretion of riboflavin was more than twice that of age- and sex-matched pair-fed control rats, and (c) after administration of chlorpromazine for a 7-wk period, tissue levels of flavin mononucleotide and FAD were significantly lower than those of pair-fed littermates, despite consumption of a diet estimated to contain 30 times the recommended dietary allowance. The present study suggests that certain psychotropic drugs interfere with riboflavin metabolism at least in part by inhibiting the conversion of riboflavin to its coenzyme derivatives, and that as a consequence of such inhibition, the overall utilization of the vitamin is impaired.
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