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[辐射诱导的基因组不稳定:现象、分子机制及致病意义]

[Radiation-induced genomic instability: phenomenon, molecular mechanisms, pathogenetic significance].

作者信息

Mazurik V K, Mikhaĭlov V F

机构信息

State Research Centre of Russia-Institute of Biophysical, Moscow, 123182, Russia.

出版信息

Radiats Biol Radioecol. 2001 May-Jun;41(3):272-89.

PMID:11458641
Abstract

The recent data on the radiation-induced genome instability as a special state of progeny of cells irradiated in vitro as well as after a whole body exposure to ionizing radiation, that make these cells considerably different from normal, unirradiated cells, were considered. This state presents a number of cytogenetical, molecular-biological, cytological and biochemical manifestations untypical for normal cells. The state is controlled by the mechanisms of regulation of checkpoints of cell cycle, and apoptosis, that is under gene p53 control. The proof has been found that this state transfers from irradiated maternal cells to their surviving progeny by the epigenetical mechanisms and would exist until the cells restore the original state of response on the DNA damage. From the point of view of the genome instability conception, that considers the chromatine rearrangement as the adaptive-evolution mechanism of adaptation of the species to changeable environmental conditions, the radiation-induced genome instability may be considered as transition of irradiated progeny to the state of read these to adaptation changes with two alternative pathways. The first leads to adaptation to enviromental conditions and restoring of normal cell functions. The second presents the cell transition into the transformed state with remain genome instability and with increase of tumour growth probability.

摘要

本文考虑了近期有关辐射诱导基因组不稳定的数据,这种不稳定是体外照射细胞以及全身暴露于电离辐射后子代细胞的一种特殊状态,使得这些细胞与正常未照射细胞有很大不同。这种状态呈现出许多正常细胞所不具备的细胞遗传学、分子生物学、细胞学和生物化学表现。该状态受细胞周期检查点和细胞凋亡调控机制的控制,而这一调控机制受p53基因控制。有证据表明,这种状态通过表观遗传机制从受照射的母细胞传递给其存活的子代,并将一直存在,直到细胞恢复对DNA损伤的原始反应状态。从基因组不稳定概念的角度来看,该概念将染色质重排视为物种适应多变环境条件的适应性进化机制,辐射诱导的基因组不稳定可被视为受照射子代向准备适应变化的状态转变,有两条替代途径。第一条途径导致对环境条件的适应和正常细胞功能的恢复。第二条途径则是细胞转变为转化状态,基因组不稳定持续存在且肿瘤生长概率增加。

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Clonal diversity and rare phenes in Taraxacum officinale s.l. coenopopulations from the East-Ural radioactive trace zone.
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