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邓承宗等, . 1992: 喜树碱对人类巨细胞病毒诱发染色体畸变的频率的调节效应(英文). 动物学研究, 13(2): 185-192.
引用本文: 邓承宗等, . 1992: 喜树碱对人类巨细胞病毒诱发染色体畸变的频率的调节效应(英文). 动物学研究, 13(2): 185-192.
DENG Cheng-zong, Sazaly AbuBakar, Michael P.Fons, Istvan Boldogh, Thomas Albrecht. 1992. Modulation of The Frequency of Human Cytomegalovirus-Induced Chromosome Aberrations by Camptothecin. Zoological Research, 13(2): 185-192.
Citation: DENG Cheng-zong, Sazaly AbuBakar, Michael P.Fons, Istvan Boldogh, Thomas Albrecht. 1992. Modulation of The Frequency of Human Cytomegalovirus-Induced Chromosome Aberrations by Camptothecin. Zoological Research, 13(2): 185-192.

喜树碱对人类巨细胞病毒诱发染色体畸变的频率的调节效应(英文)

Modulation of The Frequency of Human Cytomegalovirus-Induced Chromosome Aberrations by Camptothecin

  • 摘要: 本文评价了所选用的DNA修复抑制剂对人类巨细胞病毒(HCMV)诱发外周血淋巴细胞(PBLs)染色体畸变频率的影响。以拓扑酶I的一种抑制剂——喜树碱(0.05-0.3 ug/ml)处理HCMV感染的人类PBLs30小时,结果导致HCMV诱发的染色体损伤频率显著的协同性增加(P<0.01)。另一方面以ADP核糖聚合酶的一种抑制剂——3-氨基苯酰胺(3-AB)(3-30 ug/ml),或者拓扑酶II的一种抑制剂——新霉素(3-30 ug/ml)处理HCMV感染的PBLs30小时,染色体损伤频率未见明显增加。在喜树碱处理的HCMV感染细胞中,染色单体型断裂包括染色体交换是染色体畸变的主要类型,这提示HCMV感染与单链NDA断裂有关,这些发现还提示,HCMV感染不会造成通过3-AB或新霉素敏感途径修复的直接DNA损伤。

     

    Abstract: The effects of selected DNA repair inhibitors on the frequency of human cytomegalovirus (HCMV)-induced chromosome aberrations in human peripheral blood lymphocytes (PBLs) were evaluated.Treatment of HCMV-infected PBLs with camptothecin (0.05 to 0.3 μg/ml),an inhibitor of topoisomerase Ⅰ,for 30 hr resulted in a significant (P<0.01) synergistic enhancement of the frequency of HCMV-induced chromosome damage.On the other hand,a significant increase in the frequency of chromosome damage was not noted for infected PBLs treated with either 3-aminobenzamide (3-AB) (3 to 30 μg/ml),an inhibitor of poly (ADP-ribose) polymerase,or novobiocin (3 to 30 μg/ml) an inhibitor of topoisomerase Ⅱ or excision repair processes for 30 hr.Chromatid-type breaks including chromosome exchanges were the predominant type of chromosome aberrations observed in the HCMV-infected cells treated with camptothecin suggesting that HCMV infection is associated with the induction of single-strand DNA breaks.Furthermors,these findings suggest that HCMV infection does not inflict direct DNA damage which is repaired through 3-AB-or novobiecinsensitive pathways.

     

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