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增殖性和静止性肿瘤细胞中DNA修复动力学的调控

Regulation of DNA repair kinetics in proliferative and quiescent tumor cells.

作者信息

Wheeler K T, Nelson G B, Terrell K E, Wallen C A

机构信息

Department of Radiology, Wake Forest University Medical Center, Winston-Salem, NC 27103.

出版信息

Int J Radiat Biol. 1988 Aug;54(2):245-55. doi: 10.1080/09553008814551681.

Abstract

The radiosensitivity and kinetics of repair of radiation-induced DNA damage were determined for proliferative (P) and quiescent (Q) cells of the mouse mammary adenocarcinoma line 67. 67 Q cells are more radiosensitive than 67 P cells. Radiation induced the same amount of DNA damage in both 67 P and 67 Q cells. Both 67 P and 67 Q cells repaired their DNA damage with biphasic kinetics, but the half-times for the fast and slow phase were longer in 67 Q cells. Q cell DNA appeared to be in a more compact or condensed chromatin structure and was less accessible to enzymatic digestion than P cell DNA. These data suggest that 67 Q cells are more sensitive to ionizing radiation than 67 P cells because they repair their radiation-induced DNA damage more slowly, perhaps as a result of their more condensed chromatin structure.

摘要

测定了小鼠乳腺腺癌67系增殖性(P)细胞和静止性(Q)细胞对辐射诱导的DNA损伤的放射敏感性及修复动力学。67 Q细胞比67 P细胞对辐射更敏感。辐射在67 P细胞和67 Q细胞中诱导的DNA损伤量相同。67 P细胞和67 Q细胞均以双相动力学修复其DNA损伤,但67 Q细胞快速和慢速阶段的半衰期更长。与P细胞DNA相比,Q细胞DNA似乎处于更紧密或浓缩的染色质结构中,且更不易被酶消化。这些数据表明,67 Q细胞比67 P细胞对电离辐射更敏感,因为它们修复辐射诱导的DNA损伤更慢,这可能是由于其染色质结构更浓缩的结果。

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