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DNA氧化性损伤与端粒缩短
引用本文:赵晨阳,郑荣梁.DNA氧化性损伤与端粒缩短[J].生物化学与生物物理进展,2000,27(4):351-353.
作者姓名:赵晨阳  郑荣梁
作者单位:兰州大学生物系,兰州,730000
摘    要:末端复制问题(the end replication problem)不能完全解释端粒在某些细胞分裂过程中迅速缩短的现象.40%的高压氧下细胞传代次数降低,端粒缩短速率增大,细胞出现衰老特征,端粒DNA上单链断裂积累.推测端粒缩短的主要原因在于衰老过程中或氧胁迫下端粒DNA单链断裂增多,使端粒末端单链片段在DNA复制时丢失.端粒酶和活性氧对端粒长度的正负调控作用的准确机制还有待于更深入的研究.

关 键 词:活性氧,DNA损伤,端粒,衰老,癌变
收稿时间:1999/5/10 0:00:00
修稿时间::

Oxidative DNA Damage and Telomeres Shortening
ZHAO Chen-Yang and ZHENG Rong-Liang.Oxidative DNA Damage and Telomeres Shortening[J].Progress In Biochemistry and Biophysics,2000,27(4):351-353.
Authors:ZHAO Chen-Yang and ZHENG Rong-Liang
Institution:Department of Biology, Lanzhou University, Lanzhou 730000, China;Department of Biology, Lanzhou University, Lanzhou 730000, China
Abstract:Telomeres shortening during proliferation of many cell lines can not be explained completely by the mechanism of the end replication problem. Under 40% oxygen partical pressure, cell proliferation is blocked and the rate of telomere shortening is increased. Blocked cells present senescent characteristics and accumulated single-strand breaks in telomeres. It might be speculated that accumulation of single-strand breaks and resultant loss of distal single-stranded fragments during replication could be a major cause of telomere shortening under the condition of senescence or oxidative stress. The precise mechanism of the positive or negative regulation on the telomere length by telomerase and reactive oxygen species still remains unclear.
Keywords:reactive oxygen species  DNA damage  telomere  senescence  cancer
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