Abstract
Abstract Administration of allylisopropylacetamide to rats causes a marked increase in the hepatic ribonucleic acid-dependent synthesis of δ-aminolevulinic acid synthetase as evidenced by the fact that this increase is markedly inhibited by administration of actinomycin D or 5-fluorouracil. The half-life of hepatic δ-aminolevulinic acid synthetase following puromycin administration is 67 to 72 min and is independent of the level of the enzyme. The administration of actinomycin D or 5-fluorouracil to rats previously treated with allylisopropylacetamide results in a rapid decline of the hepatic levels of induced δ-aminolevulinic acid synthetase. This suggests that the turnover of the messenger RNA for hepatic δ-aminolevulinic acid synthetase is considerably more rapid than the bulk of rat liver messenger RNA. Glucose markedly inhibits induction of hepatic δ-aminolevulinic acid synthetase and also the increase of δ-aminolevulinic acid dehydratase produced by allylisopropylacetamide administration.
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