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非毒性剂量重金属锑通过改变细胞脂代谢促进前列腺癌进展
引用本文:李晓建,姜行康,高明,孔佑胜,潘东亮,李宁忱,#,刘思金.非毒性剂量重金属锑通过改变细胞脂代谢促进前列腺癌进展[J].生态毒理学报,2015,10(6):129-135.
作者姓名:李晓建  姜行康  高明  孔佑胜  潘东亮  李宁忱  #  刘思金
作者单位:1. 北京大学首钢医院泌尿外科,北京100144; 中国科学院生态环境研究中心,北京100085;2. 中国科学院生态环境研究中心,北京100085; 天津医科大学第二医院泌尿外科,天津市泌尿外科研究所,天津300211;3. 中国科学院生态环境研究中心,北京,100085;4. 北京大学首钢医院检验科,北京,100144;5. 北京大学首钢医院泌尿外科,北京,100144
基金项目:中国科学院环境化学与生态毒理学国家重点实验室开放基金(KF2011-12)
摘    要:本文旨在检测健康人群与前列腺癌患者血清中重金属锑的含量,并对重金属锑在前列腺癌发生发展中的作用和相关机制进行初步探索。本实验使用电感耦合等离子体质谱仪(ICP-MS)对健康人群和前列腺癌患者血清中重金属锑的含量进行了检测;此外,分别通过MTT和Alamar-Blue方法对于重金属锑对人前列腺癌PC-3细胞的毒性效应进行了评价,并进一步探讨了非毒性剂量的重金属锑对前列腺癌细胞增殖能力(细胞计数及克隆形成实验)及脂类代谢过程(细胞内甘油三酯)的影响。研究结果显示:重金属锑在前列腺癌组患者血清中含量明显高于健康人群组且差异具有统计学意义;毒性实验结果表明高剂量的重金属锑能够显著抑制细胞活力且呈浓度依赖型方式,而非毒性剂量重金属锑能够显著促进前列腺癌细胞增殖,并导致细胞内甘油三酯的含量增加(P0.05)。综上所述,重金属锑在前列腺癌患者血清中具有相对较高水平,其机制可能是通过影响细胞脂类代谢从而促进前列腺癌的进展,这将对未来前列腺癌的预防和治疗提供一定的理论依据。

关 键 词:重金属    前列腺癌  脂代谢
收稿时间:2015/3/27 0:00:00
修稿时间:2015/5/18 0:00:00

Non-toxic Dose of Antimony Exposure Could Enhance the Intracellular Energy Metabolism and Promote Prostate Cancer Progression
Li Xiaojian,Jiang Xingkang,Gao Ming,Kong Yousheng,Pan Dongliang,Li Ningchen,# and Liu Sijin.Non-toxic Dose of Antimony Exposure Could Enhance the Intracellular Energy Metabolism and Promote Prostate Cancer Progression[J].Asian Journal of Ecotoxicology,2015,10(6):129-135.
Authors:Li Xiaojian  Jiang Xingkang  Gao Ming  Kong Yousheng  Pan Dongliang  Li Ningchen  # and Liu Sijin
Institution:1. Department of Urology, Peking University Shougang Hospital, Beijing 100144, China 2. Research Center For Eco-Environmental Science, Chinese Academy of Science, Beijing 100085, China 3. Department of Urology, The Second Hospital of Tianjin Medical University, Tianjin Institute of Urology, Tianjin 300211, China 4. Department of Clinical Laboratory, Peking University Shougang hospital, Beijing 100144, China;1. Department of Urology, Peking University Shougang Hospital, Beijing 100144, China 2. Research Center For Eco-Environmental Science, Chinese Academy of Science, Beijing 100085, China 3. Department of Urology, The Second Hospital of Tianjin Medical University, Tianjin Institute of Urology, Tianjin 300211, China 4. Department of Clinical Laboratory, Peking University Shougang hospital, Beijing 100144, China;1. Department of Urology, Peking University Shougang Hospital, Beijing 100144, China 2. Research Center For Eco-Environmental Science, Chinese Academy of Science, Beijing 100085, China 3. Department of Urology, The Second Hospital of Tianjin Medical University, Tianjin Institute of Urology, Tianjin 300211, China 4. Department of Clinical Laboratory, Peking University Shougang hospital, Beijing 100144, China;1. Department of Urology, Peking University Shougang Hospital, Beijing 100144, China 2. Research Center For Eco-Environmental Science, Chinese Academy of Science, Beijing 100085, China 3. Department of Urology, The Second Hospital of Tianjin Medical University, Tianjin Institute of Urology, Tianjin 300211, China 4. Department of Clinical Laboratory, Peking University Shougang hospital, Beijing 100144, China;1. Department of Urology, Peking University Shougang Hospital, Beijing 100144, China 2. Research Center For Eco-Environmental Science, Chinese Academy of Science, Beijing 100085, China 3. Department of Urology, The Second Hospital of Tianjin Medical University, Tianjin Institute of Urology, Tianjin 300211, China 4. Department of Clinical Laboratory, Peking University Shougang hospital, Beijing 100144, China;1. Department of Urology, Peking University Shougang Hospital, Beijing 100144, China 2. Research Center For Eco-Environmental Science, Chinese Academy of Science, Beijing 100085, China 3. Department of Urology, The Second Hospital of Tianjin Medical University, Tianjin Institute of Urology, Tianjin 300211, China 4. Department of Clinical Laboratory, Peking University Shougang hospital, Beijing 100144, China;1. Department of Urology, Peking University Shougang Hospital, Beijing 100144, China 2. Research Center For Eco-Environmental Science, Chinese Academy of Science, Beijing 100085, China 3. Department of Urology, The Second Hospital of Tianjin Medical University, Tianjin Institute of Urology, Tianjin 300211, China 4. Department of Clinical Laboratory, Peking University Shougang hospital, Beijing 100144, China
Abstract:This article was aimed to detect antimony content in the serum of healthy controls (HC) and prostate cancer (PCa) patients, and investigate the role and molecular mechanisms of antimony-induced PCa progression. We analyzed the concentration of antimony in the serum of HC and PCa patients with ICP-MS, and evaluated the toxicity effect of antimony on PC3 cells by MTT and Alamar-blue assay. In addition, the cell proliferation (cell counting and colony formation tests) and lipid metabolism rates (determined by intracellular triglyceride production) of PC-3 cells in response to non-toxic dose of antimony exposures were also analyzed. And our results showed that the serum concentration of antimony in PCa patients were significantly higher than those in healthy controls (P<0.05), and high dose of antimony could markedly inhibit cell viability in a dose dependent manner. However, cell proliferation rates and intracellular triglyceride levels of PC-3 cells were all obviously enhanced in response to non-toxic dose of antimony (P<0.05). Taken together, our results suggested that serum antimony content was relatively higher in PCa patients than in those of healthy controls, and the mechanism may be attributed to that accelerated intracellular lipid metabolism (especially to triglyceride metabolism) rate promoted the progression of PCa when in response to antimony. Thus, our results may provide a promising clue for the prevention and treatment of PCa in the future.
Keywords:prostate cancer  heavy metals  antimony  lipid metabolism
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