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Animal experiment demonstrates rapid turnover and glucose repression of hepatic aminolevulinic acid synthetase in rats, indicating high instability of its messenger RNA.
Administration of allylisopropylacetamide to rats causes a marked increase in the hepatic ribonucleic acid-dependent synthesis of &aminolevulinic acid synthetase as evidenced by the fact that this increase is markedly inhibited by administration of actinomycin D or S-fluorouracil.The half-life of hepatic 6aminolevulinic acid synthetase following puromycin administration is 67 to 72 mm 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 b-aminolevulinic acid synthetase.This suggests that the turnover of the messenger RNA for hepatic &aminolevulinic acid synthetase is considerably more rapid than the bulk of rat liver messenger RNA.Glucose markedly inhibits induction of hepatic &aminolevulinic acid synthetase and also the increase of &amino-Ievulinic acid dehydratase produced by ahyhsopropylacetamide administration.
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Marver et al. (1966) studied this question.
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