Kaliman P A, Belovetskaia I V
Biokhimiia. 1986 Aug;51(8):1302-7.
The effects of actinomycin D and cycloheximide on the original and CoCl2-induced delta-aminolevulinate-synthase and heme-oxygenase activities in rat liver were investigated. It was shown that 1.5 hours after CoCl2 administration the delta-aminolevulinate-synthase activity diminishes, then increases up to the original level within the subsequent 4.5 hours, showing a further increase thereafter. The heme-oxygenase activity does not change within 1,5 hours and is then increased. Actinomycin D and cycloheximide suppress the increase in the CoCl2-induced heme-oxygenase activity, whereas that of the delta-aminolevulinate-synthase activity is blocked only by cycloheximide. Hence, the increase in the CoCl2-induced delta-aminolevulinate-synthase activity in the liver is a result of activation of translation. The degree of tryptophan pyrrolase saturation with heme decreases already by the 6th hour, whereas the level of heme in liver mitochondria and microsomes decreases only by the 15th hour following CoCl2 injection. The heme content in the liver shows a further decrease irrespective of the increase in the delta-aminolevulinate synthase activity induced by CoCl2. It may be concluded that under the given experimental conditions this enzyme is not a rate-limiting step in the terminal reaction of heme biosynthesis.
研究了放线菌素D和环己酰亚胺对大鼠肝脏中原发性和CoCl₂诱导的δ-氨基-γ-酮戊酸合酶及血红素加氧酶活性的影响。结果表明,给予CoCl₂后1.5小时,δ-氨基-γ-酮戊酸合酶活性降低,随后在接下来的4.5小时内升高至原始水平,此后进一步升高。血红素加氧酶活性在1.5小时内无变化,随后升高。放线菌素D和环己酰亚胺抑制CoCl₂诱导的血红素加氧酶活性的升高,而δ-氨基-γ-酮戊酸合酶活性的升高仅被环己酰亚胺阻断。因此,肝脏中CoCl₂诱导的δ-氨基-γ-酮戊酸合酶活性的升高是翻译激活的结果。到第6小时,色氨酸吡咯酶的血红素饱和程度已经降低,而CoCl₂注射后15小时肝脏线粒体和微粒体中的血红素水平才降低。无论CoCl₂诱导的δ-氨基-γ-酮戊酸合酶活性如何升高,肝脏中的血红素含量都进一步降低。可以得出结论:在给定的实验条件下,该酶不是血红素生物合成终末反应中的限速步骤。