[Liver reactivity to glucocorticoids in the process of chemical hepatic carcinogenesis].
The rat hepatocytes during chemical carcinogenesis (3'-MDAB), as well as the cells of chemically-induced primary rat hepatomas preserved their response to partial hepatectomy by stimulation of the 3H-thymidine incorporation into DNA; as in the normal liver this process is inhibited by dexamethason. No impairment in the inducibility of tyrosine aminotranspherase (EC.2.6.1.5) by the hormone was observed, whereas the hormonal induction of tryptophane pyrrolase (EC.1.13.11.11) in primary hepatomas was lost completely. The problem of the adequacy of the model of chemical carcinogenesis of the organ without consideration of the cell populations heterogeneity is discussed.
D000818:Animals; D004273:DNA, Neoplasm / Q000096:biosynthesis; D003907:Dexamethasone / Q000494:pharmacology; D004790:Enzyme Induction / Q000187:drug effects; D005938:Glucocorticoids / Q000494:pharmacology*; D006498:Hepatectomy; D050503:Indoleamine-Pyrrole 2,3,-Dioxygenase; D008099:Liver / Q000187:drug effects*; D008114:Liver Neoplasms, Experimental / Q000139:chemically induced*; D008297:Male; D008749:Methyldimethylaminoazobenzene; D051381:Rats; D013936:Thymidine / Q000378:metabolism; D013997:Time Factors; D014366:Tryptophan Oxygenase / Q000096:biosynthesis; D014444:Tyrosine Transaminase / Q000096:biosynthesis
D004273:DNA, Neoplasm; D005938:Glucocorticoids; D050503:Indoleamine-Pyrrole 2,3,-Dioxygenase; D008749:Methyldimethylaminoazobenzene; D003907:Dexamethasone; D014366:Tryptophan Oxygenase; D014444:Tyrosine Transaminase; D013936:Thymidine
Reaktivnost' pecheni k gliukokortikoidam v protsesse khimicheskogo gepatokantserogeneza.