Experimental Biology and Medicine · 1972 · 17 citations · 0 references
PharmacyPharmacologyToxicologyHepatotoxicologyPharmaceutical ToxicologySteroid BiochemistryBiliary ExcretionChemical-induced HepatotoxicityCholestatic Liver InjuryHepatic ToxicityHepatotoxicity MechanismsLiver DiseaseBile Acid ToxicityBile Acid-conjugated MetabolitesBile Acid-induced CholestasisHepatic Microsomal MetabolismMicrosomal Enzyme ActivityMicrosomal Enzyme-mediated Metabolism
SummaryExperiments on rats indicate that lithocholic acid-induced changes in the liver and choledochus, as well as the associated bile concrement formation, icterus, loss of body weight and mortality, are all inhibited or abolished by certain catatoxic steroids (PCN and CS-1) as well as by thyroxine and triiodothyronine. Prednisolone and triamcinolone have an opposite effect. Among the classic hepatic microsomal enzyme inducers, diphenylhydantoin is ineffective, and phenobarbital is much less potent than PCN or CS-1 in influencing the toxicity of lithocholic acid.The author thanks the Companies listed in the Materials and Methods section for kindly donating the compounds used in this experiment.