Actinomycin D-sensitive induction of choline kinase by carbon tetrachloride intoxication in rat liver.
A single intraperitoneal dose(1 ml/kg body weight) of carbon tetrachloride (CCl4) caused a rapid and drastic induction of choline kinase activity in rat liver cytosol. The administration of either cycloheximide or actinomycin D completely blocked the CCl4-mediated induction of choline kinase activity, indicating that the elevated activity could be due to the change in the enzyme level. The pretreatment of rats with phenobarbital did not cause any significant effect on hepatic choline kinase induction by CCl4, suggesting that the induction may not be directly related to the metabolic rate of CCl4. A considerable part of induced form(s) of choline kinase appeared not to be a form present in the liver of untreated rats. The contribution of adrenals to the CCl4-mediated hepatic choline kinase induction could be ruled out.
D000315:Adrenalectomy; D000818:Animals; D002252:Carbon Tetrachloride Poisoning / Q000201:enzymology*; D002797:Choline Kinase / Q000096:biosynthesis*; D003609:Dactinomycin / Q000494:pharmacology*; D004790:Enzyme Induction; D008099:Liver / Q000187:drug effects / Q000201:enzymology*; D008297:Male; D010770:Phosphotransferases / Q000096:biosynthesis*; D051381:Rats; D011919:Rats, Inbred Strains
D003609:Dactinomycin; D010770:Phosphotransferases; D002797:Choline Kinase