Fomina M M, Bogoslovskaia E P, Konradov A A, Ostrovskaia L A
Eksp Onkol. 1986;8(3):70-4.
The dimetinur effect upon chromosomes of the Ehrlich ascite carcinoma and bone marrow cell populations was analyzed by the cytogenetic method for 10 days after i.p. and i. v. drug administration in doses from 50 to 150 mg/kg. Kinetic regularities of changes in a fraction of cells with chromosome breakages and in the number of broken chromosomes per cell as well as "dose-effect" relations are determined. A linear correlation is established between the level of residual chromosome damages in a population of tumour cells and the coefficient of activity chi* characterizing the antitumour effect of dimetinur. Selectivity of the dimetinur mutagenic action expressed as a more deep and prolonged damage of the genetic system of tumour cells as compared to bone marrow cells of tumour-bearing animals is shown under conditions of a pronounced therapeutic activity.
采用细胞遗传学方法,分析了腹腔注射和静脉注射剂量为50至150mg/kg的二甲基硝基亚硝胍(dimetinur)10天后,其对艾氏腹水癌染色体及骨髓细胞群体的影响。确定了具有染色体断裂的细胞比例、每个细胞中断裂染色体数量变化的动力学规律以及“剂量-效应”关系。肿瘤细胞群体中残余染色体损伤水平与表征二甲基硝基亚硝胍抗肿瘤作用的活性系数χ*之间建立了线性相关性。在显著治疗活性的条件下,显示出二甲基硝基亚硝胍诱变作用的选择性,即与荷瘤动物的骨髓细胞相比,肿瘤细胞的遗传系统受到更深刻和持久的损伤。