Mar 1, 1976

The repression and derepression of hepatic tyrosine aminotransferase by carcinogens

Chemico-biological Interactions
M Hanausek-WalaszekT E Webb


Like hydrocortisone, a single carcinogenic dose of dimethylnitrosamine (50 mg/kg) initiates the induction cycle for hepatic tyrosine aminotransferase in adrenalectomized rats. However, following this initial induction in the presence of dimethylnitrosamine, the enzyme becomes refractory to reinduction by known inducers. The administration of thioacetamide to either adrenalectomized or intact rats leads to an immediate and progressive loss of inducibility by hydrocortisone, dibutyrylcyclic AMP or dimethylnitrosamine. Although the thioacetamide-induced repression was not reversed even up to 10 weekds after the cessation of treatment, it was reversed after the induction of liver regeneration. Both the carcinogen-mediated induction and repression of tyrosine aminotransferase appears to occur by mechanisms which do not involve the corticosteroid-binding proteins which normally mediate the induction by glucocorticoids.

Mentioned in this Paper

Glucocorticoid inhalants for obstructive airway disease
Corticosteroid [EPC]
Tyrosine Aminotransferase
Glucocorticoids, Systemic
Liver Diseases
Adrenal Cortex Hormones
Binding Protein

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