Mayer V W, Hybner C J, Brusick D J
Mutat Res. 1976 Nov;37(2-3):201-12. doi: 10.1016/0027-5107(76)90034-8.
Cyclophosphamide induced forward mutation in Saccharomyces cerevisiae strain S288C and mitotic recombination in strains D3 and D5 but not in strain D4. The yeast cells were treated with the compound in phosphate buffer without recourse to metabolic activation protocols. Elevation of the treatment temperature increased the genetic activity of cyclophosphamide. Respiration-deficient isolates of strains S288C and D3 were more sensitive than the respiratory competent parent strains were for inducing forward mutation and mitotic recombination, respectively. Cyclophosphamide was incubated in phosphate buffer alone for increasing time intervals; strain D3 cells were added to aliquots for each time interval and incubated for an additional 30 min. The frequency of induced recombination increased as the time of compound incubation increased, showing that spontaneous degradation of cyclophosphamide to genetically active breakdown products was responsible for the genetic damage induced in the yeast cells.
环磷酰胺在酿酒酵母菌株S288C中诱导正向突变，在菌株D3和D5中诱导有丝分裂重组，但在菌株D4中未诱导。酵母细胞在磷酸盐缓冲液中用该化合物处理，无需借助代谢活化方案。提高处理温度会增加环磷酰胺的遗传活性。菌株S288C和D3的呼吸缺陷型分离株分别比呼吸正常的亲本菌株对诱导正向突变和有丝分裂重组更敏感。环磷酰胺在单独的磷酸盐缓冲液中孵育不同时间间隔；将菌株D3细胞加入每个时间间隔的等分试样中，并再孵育30分钟。随着化合物孵育时间的增加，诱导重组的频率增加，表明环磷酰胺自发降解为具有遗传活性的分解产物是酵母细胞中诱导遗传损伤的原因。
