[Jurkat细胞系γ诱导死亡的机制]

[Mechanisms of gamma-inducible death of Jurkat cells line].

作者信息

Gamkrelidze M M, Bezhitashvili N D, Pavliashvili A T, Mchedlishvili T V, Sanikidze T V

出版信息

Georgian Med News. 2008 Jun(159):58-61.

Abstract

Mechanisms of radio-inducible death of Jurkat cells were investigated. Human lymphoblastoid T-cell line Jurkat is widely established model for studying apoptosis mechanisms. The cell was radiated by "Teragam" (Czech Republic) by dose 2 g during 1 minute. After radiation cells were incubated at standard conditions during 24 hours. After gamma radiation in cell population amount of cells in gaplois (apoptotic G 0) stage was increased 8,2 folds, in diplois (G 0/G1) stage - by 17%, in synthetic (S) stage decreased by 35% and tetraploid (G2/M) stage by 73% in comparison to control group. It was revealed intensive production of free radicals of oxygen and nitric oxide and decreasing activity of antioxidant enzymes (superoxidismutasa, catalasa and glutathione peroxidase). Revealed dependence between intensification of apoptosis and radiation-induced arrest of cell cycle G2/M phase may be determined by excess amount of free oxygen and nitrogen radicals generated in Jurkat cells as a result of nondirect effects of low doses of gamma radiation.

摘要

对Jurkat细胞的辐射诱导死亡机制进行了研究。人淋巴母细胞T细胞系Jurkat是研究凋亡机制广泛应用的模型。细胞用来自捷克共和国的“Teragam”以2戈瑞的剂量照射1分钟。照射后，细胞在标准条件下孵育24小时。与对照组相比，γ射线照射后，处于间隙期（凋亡G0期）的细胞数量增加了8.2倍，二倍体（G0/G1期）的细胞数量增加了17%，合成期（S期）的细胞数量减少了35%，四倍体（G2/M期）的细胞数量减少了73%。研究发现，氧自由基和一氧化氮大量产生，抗氧化酶（超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶）的活性降低。凋亡加剧与辐射诱导的细胞周期G2/M期阻滞之间的相关性，可能是由于低剂量γ射线的非直接效应导致Jurkat细胞中产生过量的氧自由基和氮自由基所致。