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[化学性肝癌发生过程中肝脏对糖皮质激素的反应性]

[Liver reactivity to glucocorticoids in the process of chemical hepatic carcinogenesis].

作者信息

Mechitov V I, Adler V V, Shapot V S

出版信息

Biull Eksp Biol Med. 1979 Mar;87(3):276-9.

PMID:34453
Abstract

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.

摘要

化学致癌作用(3'-甲基-4-二甲基氨基偶氮苯,3'-MDAB)过程中的大鼠肝细胞,以及化学诱导的原发性大鼠肝癌细胞,通过刺激3H-胸腺嘧啶核苷掺入DNA,保留了对部分肝切除术的反应;与正常肝脏一样,这一过程受到地塞米松的抑制。未观察到激素对酪氨酸转氨酶(EC.2.6.1.5)诱导能力的损害,而原发性肝癌中色氨酸吡咯酶(EC.1.13.11.11)的激素诱导作用则完全丧失。讨论了不考虑细胞群体异质性的器官化学致癌模型的适用性问题。

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