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在存在ADP-核糖基化抑制剂的情况下,来自N-甲基-N'-硝基-N-亚硝基胍的分裂和汇合C3H10T1/2细胞的细胞恢复。

Cellular recovery of dividing and confluent C3H10T1/2 cells from N-methyl-N'-nitro-N-nitrosoguanidine in the presence of ADP-ribosylation inhibitors.

作者信息

Jacobson E L, Smith J Y, Wielckens K, Hilz H, Jacobson M K

出版信息

Carcinogenesis. 1985 May;6(5):715-8. doi: 10.1093/carcin/6.5.715.

DOI:10.1093/carcin/6.5.715
PMID:2988808
Abstract

The relationship between treatment with 3-methoxy-benzamide (MBA), a potent inhibitor of ADP-ribosylation reactions, and the response of C3H10T1/2 cells to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) has been examined. Quiescent cells effected potentially lethal damage repair (PLDR) over a 48-h period following MNNG and the repair was coincident with the removal of DNA strand breaks. MBA had no effect on PLDR but was very co-cytotoxic with MNNG in dividing cells. The presence of MBA caused the appearance of an additional number of DNA strand breaks following MNNG in both quiescent and dividing cells. These results suggest that ADP-ribosylation is required for normal cell cycle progression following DNA damage in dividing cells.

摘要

已对3-甲氧基苯甲酰胺(MBA,一种有效的ADP-核糖基化反应抑制剂)的处理与C3H10T1/2细胞对N-甲基-N'-硝基-N-亚硝基胍(MNNG)的反应之间的关系进行了研究。静止细胞在MNNG处理后的48小时内进行潜在致死性损伤修复(PLDR),且这种修复与DNA链断裂的消除同时发生。MBA对PLDR没有影响,但在分裂细胞中与MNNG具有很强的共细胞毒性。MBA的存在导致在静止细胞和分裂细胞中MNNG处理后出现额外数量的DNA链断裂。这些结果表明,ADP-核糖基化对于分裂细胞中DNA损伤后的正常细胞周期进程是必需的。

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