Barone C, Gentiloni N, Bartoloni C, Gambassi G, Terranova T
Oncology. 1979;36(1):1-6. doi: 10.1159/000225308.
Microsomal cytochromes and some oxidative activities were determined in normal rat liver, tumour-bearing rat liver and Morris hepatoma 3924-A. Except for a moderate lowering of cytochromes and enzymes in host livers, the relation between TPNH-cytochrome c reductase activity and cytochrome P-450 TPNH reduction, both increased by phenobarbital (PB) and decreased by 3-methylcolanthrene (3-MC) treatment, is noteworthy. In tumour cytochromes b5 and P-450 are absent and TPNH-cytochrome c reductase is unmeasurable and not induced by PB or 3-MC treatment. Aminopyrine demethylase activity, instead, is comparable with normal or host liver and it is modified by PB or 3-MC treatment in the same way, despite the microsomal enzymes pathway disorganization. Microsomal enzymatic defect selectivity in tumours may be due to a deranged microsome-linked growth control.
在正常大鼠肝脏、荷瘤大鼠肝脏和莫里斯肝癌3924 - A中测定了微粒体细胞色素和一些氧化活性。除宿主肝脏中细胞色素和酶有适度降低外，值得注意的是，经苯巴比妥（PB）处理后增加、经3 - 甲基胆蒽（3 - MC）处理后降低的三磷酸吡啶核苷酸 - 细胞色素c还原酶活性与细胞色素P - 450三磷酸吡啶核苷酸还原之间的关系。在肿瘤中，细胞色素b5和P - 450缺失，三磷酸吡啶核苷酸 - 细胞色素c还原酶无法测定，且不受PB或3 - MC处理诱导。相反，氨基比林脱甲基酶活性与正常或宿主肝脏相当，尽管微粒体酶途径紊乱，但它经PB或3 - MC处理后的变化方式相同。肿瘤中微粒体酶缺陷的选择性可能是由于与微粒体相关的生长控制紊乱所致。
