Barranco S C, Novak J K, Humphrey R M
Cancer Res. 1975 May;35(5):1194-204.
The survival of plateau-phase or nondividing Chinese hamster ovary cells (in vitro) is reduced to a greater extent by treatments with nitrosourea compounds than are cells treated in the exponential phase of growth. The greatest decrease in the survival fraction occurred following treatments with 1-trans-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea where approximately 128 times more cells were killed in plateau phase than in the dividing state (at the 10 mug/ml-for-1-hr dose). Only 5 times more cells were killed in plateau phase than in exponential growth when cells were treated with 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea. Cells treated with either nitrosourea compound failed to recover from potentially lethal damage and sublethal damage. The breakdown products of the nitrosourea compounds are known to inhibit DNA repair and may explain the failure of mammalian cells to recover from sublethal damage and potentially lethal damage induced by these chemicals. Both dividing and nondividing cells were able to recover from bleomycin-induced potentially lethal damage but not from sublethal damage. The recovery from bleomycin-induced potentially lethal damage by nondividing cells was twice as great as that exhibited by dividing cells; however, potentially lethal damage recovery was suffieiently high for cells in both growth states to conceal the true response to sublethal damage.
与处于指数生长期的细胞相比，亚硝基脲化合物处理对处于平台期或不分裂的中国仓鼠卵巢细胞（体外）的存活率降低程度更大。在用1-反式-（2-氯乙基）-3-（4-甲基环己基）-1-亚硝基脲处理后，存活分数下降最大，在平台期被杀死的细胞数量大约是分裂状态下（在10微克/毫升处理1小时的剂量下）的128倍。当用1-（2-氯乙基）-3-环己基-1-亚硝基脲处理时，平台期被杀死的细胞数量仅比指数生长期多5倍。用这两种亚硝基脲化合物处理的细胞均未能从潜在致死损伤和亚致死损伤中恢复。已知亚硝基脲化合物的分解产物会抑制DNA修复，这可能解释了哺乳动物细胞无法从这些化学物质诱导的亚致死损伤和潜在致死损伤中恢复的原因。分裂细胞和不分裂细胞都能够从博来霉素诱导的潜在致死损伤中恢复，但不能从亚致死损伤中恢复。不分裂细胞从博来霉素诱导的潜在致死损伤中的恢复程度是分裂细胞的两倍；然而，两种生长状态下细胞的潜在致死损伤恢复程度都足够高，从而掩盖了对亚致死损伤的真实反应。
