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The paradoxical effect of hydrocortisone and actinomycin on the activity of rabbit leucocyte alkaline phosphatase

1967; Elsevier BV; Volume: 26; Issue: 3 Linguagem: Inglês

10.1016/0006-291x(67)90116-7

1090-2104

E.E. McCoy, M. Ebadi,

Parathyroid Disorders and Treatments

Administration of actinomycin D to fasted rats induces an enhancement of the labeling of hepatic ubiquinone by [2-14C] acetate both in vivo and in vitro. The incorporation of [2-14C] mevalonate into ubiquinone is also increased, although to a significantly lesser extent; this, however, presumably results from greater uptake of the labeled precursor by liver of drug-treated rats. The drug-administered animals show increased activity of liver microsomal mevalonate: NADP oxidoreductase, the rate-limiting enzyme in isoprenoid biogenesis.The incorporation of [U-14C] benzoic acid and CH3-[14C]methionine into ubiquinone in liver slices, however, reveals a decrease in actinomycin D administered rats. This appears to be due to a specific inhibition of the pathway leading to the benzoquinone moiety of ubiquinone and not to an increase in the pool-size of the precursors.The stimulatory effect of the drug on ubiquinone biosynthesis is also observable in cholesterol-fed rats. The actinomycin D-induced increase in ubiquinone biosynthesis is dependent on new protein synthesis since the effect is abolished by treating the animals with either cycloheximide or puromycin.