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高传能线密度辐射诱导的细胞凋亡不受细胞p53基因状态的影响。

Apoptosis induced by high-LET radiations is not affected by cellular p53 gene status.

作者信息

Takahashi A, Matsumoto H, Furusawa Y, Ohnishi K, Ishioka N, Ohnishi T

机构信息

Department of Biology, Nara Medical University School of Medicine, Nara, Japan.

出版信息

Int J Radiat Biol. 2005 Aug;81(8):581-6. doi: 10.1080/09553000500280484.

DOI:10.1080/09553000500280484
PMID:16298939
Abstract

To learn more about the biological effects of high-linear energy transfer (LET) radiations, we examined radiation-induced apoptosis in response to high-LET radiations in cells with wild-type, mutated and null p53 gene. Three human lung cancer cell lines were used. These lines had identical genotypes, except for the p53 gene. Cells were exposed to X-rays or high-LET radiations (13 - 200 keV microm(-1)) using different nuclei ion beams. Cellular radiation sensitivities were determined with the use of colony-forming assays. Apoptosis was detected and quantified using Hoechst 33342 staining with fluorescence microscopy. It was found that (1) there was no significant difference in cellular sensitivity to high-LET radiation (>85 keV microm(-1)), although the sensitivity of wild-type p53 cells to X-rays was higher than that of mutated p53 or p53-null cells; (2) X-ray-induced apoptosis at higher frequencies in wild-type p53 cells when compared with mutated p53 and p53-null cells; and (3) Fe beams (200 keV microm(-1)) induced apoptosis in a p53-independent manner. The results indicate that high-LET radiations induces apoptosis in human lung cancer cells in a manner that does not seem to depend on the p53 gene status of the cells.

摘要

为了更深入了解高传能线密度(LET)辐射的生物学效应,我们检测了野生型、突变型和p53基因缺失型细胞对高LET辐射的辐射诱导凋亡情况。使用了三个人类肺癌细胞系。除了p53基因外,这些细胞系具有相同的基因型。细胞使用不同的原子核离子束接受X射线或高LET辐射(13 - 200 keV·μm⁻¹)。通过集落形成试验测定细胞的辐射敏感性。使用Hoechst 33342染色结合荧光显微镜检测并定量凋亡情况。结果发现:(1)细胞对高LET辐射(>85 keV·μm⁻¹)的敏感性没有显著差异,尽管野生型p53细胞对X射线的敏感性高于突变型p53或p53缺失型细胞;(2)与突变型p53和p53缺失型细胞相比,野生型p53细胞中X射线诱导的凋亡频率更高;(3)铁离子束(200 keV·μm⁻¹)以一种不依赖p53的方式诱导凋亡。结果表明,高LET辐射以一种似乎不依赖于细胞p53基因状态的方式诱导人肺癌细胞凋亡。

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