小鼠FM3A细胞中的dNTP失衡与DNA双链断裂及细胞死亡机制

dNTP imbalance and DNA double strand breaks in mouse FM3A cells and the mechanism of cell death.

作者信息

Wataya Y, Watanabe K, Yoshida S, Hiramoto-Yoshioka A

机构信息

Faculty of Pharmaceutical Sciences, Okayama University, Japan.

出版信息

Nucleic Acids Symp Ser. 1989(21):11-2.

Abstract

The mechanism of intracellular deoxyribonucleoside-triphosphate (dNTP) imbalance death of mouse mammary tumor FM3A cells was studied. When the cells were exposed to 5-fluorodeoxyuridine, deoxyadenosine, or 2-chlorodeoxyadenosine, dNTP pool imbalance resulted. The imbalance was followed by DNA double-strand breaks and subsequent cell death. The DNA double strand breaks were directly examined by means of orthogonal-field-alternation gel electrophoresis (OFAGE). Fragmented DNA band appeared to be approximately 100-200 kbp in size. The bases of 5'-termini in the DNA were cytosine and thymine. The imbalance induced endonuclease has been isolated by DEAE-agarose column chromatography.

摘要

研究了小鼠乳腺肿瘤FM3A细胞的细胞内脱氧核糖核苷三磷酸（dNTP）失衡死亡机制。当细胞暴露于5-氟脱氧尿苷、脱氧腺苷或2-氯脱氧腺苷时，会导致dNTP库失衡。失衡之后是DNA双链断裂及随后的细胞死亡。通过正交交变电场凝胶电泳（OFAGE）直接检测DNA双链断裂。断裂的DNA条带大小似乎约为100 - 200 kbp。DNA 5'-末端的碱基是胞嘧啶和胸腺嘧啶。通过DEAE-琼脂糖柱色谱法分离出了失衡诱导的核酸内切酶。

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dNTP imbalance and DNA double strand breaks in mouse FM3A cells and the mechanism of cell death.小鼠FM3A细胞中的dNTP失衡与DNA双链断裂及细胞死亡机制

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