Yoshioka A, Tanaka S, Hiraoka O, Koyama Y, Hirota Y, Wataya Y
Nucleic Acids Symp Ser. 1985(16):245-8.
The mechanism of 5-fluorouracil (5-FU) and 5-fluorodeoxyuridine (FdUR)-induced death of mouse mammary tumor FM3A cells was studied. When the cells were exposed to 5-FU or FdUR, an unbalance of intracellular dNTP pool resulted. The unbalance was followed by breakage of mature DNA. DNA double strand breaks were observed in the FdUR (1 microM) treated cells 16 hrs after the administration. We assume that the double strand breaks play an important role in the mechanism of the FdUR-mediated cell death. In addition, the activity that can induce DNA double strand breaks was detected in the lysate of FdUR treated FM3A cells. Since intracellular dNTP pool unbalance seems to be the trigger of these events, this phenomenon may be termed as dNTP-unbalanced cell death.
研究了5-氟尿嘧啶（5-FU）和5-氟脱氧尿苷（FdUR）诱导小鼠乳腺肿瘤FM3A细胞死亡的机制。当细胞暴露于5-FU或FdUR时，细胞内dNTP库出现失衡。这种失衡随后导致成熟DNA断裂。在给予FdUR（1 microM）16小时后，在处理过的细胞中观察到DNA双链断裂。我们认为双链断裂在FdUR介导的细胞死亡机制中起重要作用。此外，在FdUR处理的FM3A细胞裂解物中检测到了可诱导DNA双链断裂的活性。由于细胞内dNTP库失衡似乎是这些事件的触发因素，这种现象可称为dNTP失衡性细胞死亡。
