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γ辐射可在体内诱导放射敏感细胞中Bax蛋白上调及细胞凋亡。

Gamma-radiation induces upregulation of Bax protein and apoptosis in radiosensitive cells in vivo.

作者信息

Kitada S, Krajewski S, Miyashita T, Krajewska M, Reed J C

机构信息

La Jolla Cancer Research Foundation, California 92037, USA.

出版信息

Oncogene. 1996 Jan 4;12(1):187-92.

PMID:8552390
Abstract

Lymphoid cells and small intestinal epithelial (SIE) cells are among the most radiosensitive in the body. The factors that account for the differential sensitivity to gamma-radiation among different tissue-types remain poorly understood, but can only partly be explained by differences in rates of cell proliferation. Here we demonstrate that exposure of mice to 800 cGy of gamma-radiation results in rapid elevations in the levels of the Bax protein, a pro-apoptotic member of the Bcl-2 protein family, in lymphoid cells and SIEs. gamma-Radiation-induced increase in Bax protein were evident within 2 h and persisted for at least 24 h, as determined by immunoblotting and immunohistochemical assays. Increases in Bax were followed by massive apoptosis in lymphoid organs and in the small intestinal crypts, as determined by morphological criteria and in situ end-labeling of fragmented nuclear DNA by terminal deoxynucleotidyl transferase (TUNEL method). Radiation did not induce elevations in Bax or apoptosis in radioresistant tissues such as heart, skeletal muscle, brain, kidney, liver, lung, vascular smooth muscle and connective tissue. The findings suggest that Bax may be one of the mediators of radiation-induced apoptosis in vivo.

摘要

淋巴细胞和小肠上皮(SIE)细胞是体内对辐射最敏感的细胞之一。不同组织类型对γ射线敏感性差异的原因仍知之甚少,但只能部分地用细胞增殖速率的差异来解释。在此,我们证明,给小鼠暴露于800 cGy的γ射线会导致淋巴细胞和SIE中Bax蛋白(Bcl-2蛋白家族的促凋亡成员)水平迅速升高。通过免疫印迹和免疫组织化学分析确定,γ射线诱导的Bax蛋白增加在2小时内明显,并持续至少24小时。Bax增加之后,根据形态学标准以及通过末端脱氧核苷酸转移酶对断裂的核DNA进行原位末端标记(TUNEL法)确定,淋巴器官和小肠隐窝中出现大量凋亡。辐射并未诱导心脏、骨骼肌、脑、肾、肝、肺、血管平滑肌和结缔组织等抗辐射组织中Bax升高或凋亡。这些发现表明,Bax可能是体内辐射诱导凋亡的介质之一。

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Oncogene. 1996 Jan 4;12(1):187-92.
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