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[不同传能线密度低剂量辐射对人外周血淋巴细胞的细胞遗传学效应及其可能的作用机制]

[Cytogenetic effects of low dose radiation with different LET in human peripheral blood lymphocytes and possible mechanisms of their realization].

作者信息

Nasonova E A, Shmakova N L, Komova O V, Mel'nikova L A, Fadeeva T A, Krasavin E A

出版信息

Radiats Biol Radioecol. 2006 Jul-Aug;46(4):457-60.

Abstract

The induction of chromosome damage by the exposure to low doses of gamma-(60)Co and accelerated carbon ions 12C in peripheral blood lymphocytes of different donors was investigated. The complex nonlinear dose-effect dependence at the range from 1 to 50-70 cGy was observed. At the doses of 1-5 cGy the cells show the highest radiosensitivity (hypersensitivity), mainly due to the chromatid-type aberration, which is typical to those spontaneously generated in the cell and believed not to be induced by the irradiation of unstimulated lymphocytes according to the classical theory of aberration formation. With the increasing dose the frequency of the aberrations decreases significantly, in some cases up to the control level. At the doses over 50-70 cGy the dose-effect curve becomes linear. The possible role of the oxidative stress, caused by radiation-induced increase in mitochondrial reactive oxigen species (ROS) release in the phenomenon of hypersensitivity (HS) at low doses is discussed as well as cytoprotective mechanisms causing the increased radioresistance at higher doses.

摘要

研究了不同供体外周血淋巴细胞暴露于低剂量γ-(60)Co和加速碳离子12C下染色体损伤的诱导情况。在1至50 - 70 cGy范围内观察到复杂的非线性剂量效应依赖性。在1 - 5 cGy剂量下,细胞表现出最高的放射敏感性(超敏感性),主要是由于染色单体型畸变,这在细胞中自发产生时较为典型,并且根据经典的畸变形成理论,认为未受刺激的淋巴细胞照射不会诱导这种畸变。随着剂量增加,畸变频率显著降低,在某些情况下降至对照水平。在超过50 - 70 cGy的剂量下,剂量效应曲线变为线性。还讨论了低剂量超敏感性(HS)现象中由辐射诱导的线粒体活性氧(ROS)释放增加所引起的氧化应激的可能作用,以及导致高剂量时放射抗性增加的细胞保护机制。

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