Göttlicher M, Cikryt P
Cancer Lett. 1987 Apr;35(1):65-70. doi: 10.1016/0304-3835(87)90057-7.
The induction of ornithine decarboxylase (ODC) in rat liver by the carcinogen 2-acetylaminofluorene (2AAF), the strong liver tumor initiator trans-4-acetylaminostilbene (AAS), the non-carcinogen 4-acetylaminofluorene (4AAF) and, as a control, 3-methylcholanthrene (MC) has been examined. MC and all aromatic amines increased the ODC activity of rat liver from 3.6-fold (MC) to maximal 5.7-fold (AAS). The time course of the maximal induction differs from 2.5 h (2AAF) to 10 h (MC). The cytosolic concentrations of the unchanged compounds parallel the ODC activity. These data indicate that ODC induction in rat liver shows no correlation with tumor promoting properties of the model compounds. It is concluded that the unchanged compound is responsible for the ODC induction.
已对致癌物2-乙酰氨基芴(2AAF)、强效肝肿瘤引发剂反式-4-乙酰氨基芪(AAS)、非致癌物4-乙酰氨基芴(4AAF)以及作为对照的3-甲基胆蒽(MC)对大鼠肝脏中鸟氨酸脱羧酶(ODC)的诱导作用进行了研究。MC和所有芳香胺使大鼠肝脏的ODC活性提高了3.6倍(MC)至最大5.7倍(AAS)。最大诱导的时间进程从2.5小时(2AAF)到10小时(MC)不等。未变化化合物的胞质浓度与ODC活性平行。这些数据表明,大鼠肝脏中ODC的诱导与模型化合物的促肿瘤特性无关。得出的结论是,未变化的化合物是ODC诱导的原因。