Affordable Access

Publisher Website

The repression and derepression of hepatic tyrosine aminotransferase by carcinogens

Authors
Journal
Chemico-Biological Interactions
0009-2797
Publisher
Elsevier
Volume
12
Identifiers
DOI: 10.1016/0009-2797(76)90053-3
Disciplines
  • Biology

Abstract

Abstract 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 weeks 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.

There are no comments yet on this publication. Be the first to share your thoughts.

Statistics

Seen <100 times
0 Comments

More articles like this

The repression and derepression of hepatic tyrosin...

on Chemico-Biological Interaction... March 1976

Tyrosine aminotransferase: activation or repressio...

on Proceedings of the Society for... February 1969

The regulation of hepatic tyrosine aminotransferas...

on Biochimica et Biophysica Acta Nov 05, 1981

Hepatic tyrosine aminotransferase in tyrosinaemia...

on Journal of Inherited Metabolic... 1982
More articles like this..