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博来霉素诱导的结节性硬化症中的染色体损伤。

Bleomycin-induced chromosomal damage in tuberous sclerosis.

作者信息

Vorechovsky I, Juraskova V

机构信息

Research Institute of Paediatrics, Brno, Czechoslovakia.

出版信息

Jinrui Idengaku Zasshi. 1990 Jun;35(2):207-13. doi: 10.1007/BF01876466.

Abstract

To investigate the possible involvement of mutagen-induced chromosomal instability in tuberous sclerosis the blood lymphocytes obtained from eleven patients with this disease and eleven healthy controls of comparable age and sex were exposed to bleomycin in vitro during the late S and G2 phases of the cell cycle. Neither the spontaneous aberration yields nor the bleomycin-induced chromosomal sensitivity differed between the two groups. The chromosomal distribution of 578 and 478 induced breaks in patients and controls, respectively, was similar. Thus, bleomycin-induced G2 chromosomal hypersensitivity in lymphocytes of patients with tuberous sclerosis is not an intrinsic feature of this hereditary disease.

摘要

为了研究诱变剂诱导的染色体不稳定性在结节性硬化症中可能的作用,从11例患有该病的患者以及11例年龄和性别相仿的健康对照者身上获取血液淋巴细胞,在细胞周期的S期晚期和G2期将其体外暴露于博来霉素。两组之间的自发畸变率和博来霉素诱导的染色体敏感性均无差异。患者和对照者分别有578处和478处诱导断裂的染色体分布相似。因此,博来霉素诱导的结节性硬化症患者淋巴细胞G2期染色体超敏反应并非这种遗传性疾病的固有特征。

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