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DNA合成抑制对X射线照射的L5178Y-S细胞恢复的影响,II. 9-β-D-阿拉伯呋喃糖基腺嘌呤

Effect of inhibition of DNA synthesis on recovery of X-irradiated L5178Y-S cells, II. 9-beta-D-arabinofuranosyladenine.

作者信息

Kapiszewska M, Lange C S

机构信息

Institute of Molecular Biology, Jagiellonian University, Krakow, Poland.

出版信息

Neoplasma. 1989;36(5):565-72.

PMID:2812150
Abstract

The effects of 9-beta-D-arabinofuranosyladenine (araA) on radiosensitivity, postirradiation changes in the cell cycle distribution and DNA synthesis in mouse L5178Y-S lymphoma cells are described. Increase in the araA concentration (from 25 to 200 mumol/l) was is correlated with reduction in clonogenic survival except in the low concentration range. where resistance was observed. AraA treatment (200 mumol/l for 2 h) temporarily inhibited progression through the G1/S boundary. AraA (200 mumol/l applied immediately after X-irradiation (1 Gy) for 2 h gave a radiosensitizing effect with only slight changes in postirradiation cell cycle distribution; at higher doses (4 and 6 Gy) the effect was less pronounced. AraA slowed down progression through the cell cycle after irradiation and enhances the lethal effect of radiation. The phenomenon was dependent on the time between irradiation and araA treatment. The differences in dose-related radiosensitization created araA + X-ray survival curves with extrapolation numbers lower than 1. This may reflect the existence of relatively radioresistant and radiosensitive subpopulations in the araA-treated population.

摘要

描述了9-β-D-阿拉伯呋喃糖基腺嘌呤(araA)对小鼠L5178Y-S淋巴瘤细胞放射敏感性、照射后细胞周期分布变化及DNA合成的影响。araA浓度增加(从25至200μmol/l)与克隆形成存活率降低相关,但在低浓度范围内观察到抗性。araA处理(200μmol/l,2小时)暂时抑制了细胞通过G1/S边界的进程。X射线照射(1 Gy)后立即给予araA(200μmol/l,2小时)产生放射增敏作用,照射后细胞周期分布仅有轻微变化;在较高剂量(4和6 Gy)时,这种作用不太明显。araA减缓了照射后细胞通过细胞周期的进程,并增强了辐射的致死效应。该现象取决于照射与araA处理之间的时间。剂量相关放射增敏作用的差异使得araA + X射线存活曲线的外推数低于1。这可能反映了araA处理群体中存在相对抗辐射和辐射敏感的亚群。

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