COMBINATION TREATMENT OF HYDROGEN PEROXIDE AND X-RAYS INDUCES APOPTOSIS IN HUMAN PROSTATE CANCER PC-3 CELLS
COMBINATION TREATMENT OF HYDROGEN PEROXIDE AND X-RAYS INDUCES APOPTOSIS IN HUMAN PROSTATE CANCER PC-3 CELLS
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DOI：
10.1016/j.ijrobp.2009.04.092
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发表时间：
2009-10-01
影响因子：
7
通讯作者：
Ogawa, Yasuhiro
中科院分区：
文献类型：
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作者：
Kariya, Shinji;Sawada, Ken;Ogawa, Yasuhiro
目的：研究过氧化氢(H_2O_2)对人前列腺癌PC-3细胞辐射诱导凋亡的影响。方法与材料：照射前4h，将PC-3细胞暴露于10 mM氯化铵(NH4Cl)中。结果：照射后48h，细胞凋亡率分别为1.85%、4.85%、28.4%。在X射线照射和H_2O_2联合作用下，细胞在照射后4h产生了活性氧(ROS)。这导致溶酶体破裂，线粒体碎裂，细胞色素c从线粒体释放到细胞质中。相反，在X射线照射和过氧化氢处理前暴露于NH4Cl时，细胞的凋亡几乎完全被抑制，ROS的产生没有发生，溶酶体断裂和线粒体碎裂被阻止，细胞色素c没有释放。结论：过氧化氢强烈促进了溶酶体依赖的辐射诱导的人前列腺癌PC-3细胞的凋亡。X射线和H_2O_2联合使用还可以损伤线粒体细胞器，并导致ROS的产生，而ROS本身可能会诱导细胞凋亡。(C)2009年爱思唯尔公司。
Purpose: To study the effect of hydrogen peroxide (H2O2) on radiation-induced apoptosis in human prostate cancer PC-3 cells.Methods and Materials: At 4h before the irradiation, PC-3 cells were exposed to 10mM ammonium chloride (NH4Cl) concentrations. Subsequently, cells were exposed to 0.1mM H2O2 just before the irradiations, which were administered with 10-MV X-rays at doses of 10Gy.Results: The percentage of apoptotic cells at 48h after X-irradiation alone, H2O2 alone, and combined X-irradiation and H2O2 was 1.85%, 4.85%, and 28.4%, respectively. With use of combined X-irradiation and H2O2, production of reactive oxygen species (ROS) occurred 4h after the irradiation. This resulted in lysosomal rupturing, mitochondrial fragmentation, and the release of cytochrome c into the cytoplasm from the mitochondria. In contrast, when cells were exposed to NH4Cl before the X-irradiation and H2O2 administration, apoptosis was almost completely suppressed, ROS production did not occur, lysosomal rupture and mitochondrial fragmentation were blocked, and cytochrome c was not released.Conclusions: Hydrogen peroxide strongly enhanced lysosome-dependent radiation-induced apoptosis in human prostate cancer PC-3 cells. A combined use of X-rays and H2O2 can also injure the mitochondrial cytoplasmic organelles and lead to the production of ROS that in and of itself might possibly induce apoptosis. (C) 2009 Elsevier Inc.