| 微囊藻毒素MC-LR对肝细胞毒性机理研究 |
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| 引用本文： | 施玮, 朱惠刚, 晏晓蓉, 周志俊. 微囊藻毒素MC-LR对肝细胞毒性机理研究[J]. 中国公共卫生, 2002, 18(2): 139-140. DOI: 10.11847/zgggws2002-18-02-07 |
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| 作者姓名： | 施玮 朱惠刚 晏晓蓉 周志俊 |
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| 作者单位： | 1.复旦大学公共卫生学院环境卫生学教研室 上海200032 |
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| 基金项目： | 卫生部标准委员会基金资助项目(299065)国家自然科学基金资助项目(399706280) |
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| 摘 要： | 目的 研究微囊藻毒类MC-LR的肝脏毒性机理。方法 采用四唑盐比色试验和流式细胞术检测微囊藻毒素MC-LR对原代培养的肝细胞和Hela细胞生长、细胞周期和凋亡的影晌。结果 微囊藻毒素在极低浓度时表现为抑制细胞生长或细胞毒作用,高浓度时可促进细胞生长。MC-LR导致肝细胞发生典型的凋亡样变化和细胞周期G2/M期阻滞。提示微囊藻毒素可能具有影响肝细胞周期的作用,可诱导肝细胞增殖,同时又能诱导肝细胞凋亡。流式细胞术结果表明微囊藻毒素对Hela细胞周期有类似影晌趋势,但其程度远不如对肝细胞的影响明显。结论 微囊藻毒素对肝细胞的特异性作用可能是其肝脏毒性的机理之一。
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| 关 键 词： | 四唑盐比色试验 流式细胞术 微囊藻毒素 细胞生长 细胞周期 凋亡 |
| 文章编号： | 1001-0580(2002)02-0139-02 |
| 收稿时间： | 2001-02-26 |
| 修稿时间： | 2001-02-26 |
Study on Mechanism of Hepatocyte Toxicity |
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| SHI Wei, ZHU Hui-gang, YAN Xiao-rong, . Study on Mechanism of Hepatocyte Toxicity[J]. Chinese Journal of Public Health, 2002, 18(2): 139-140. DOI: 10.11847/zgggws2002-18-02-07 |
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| Authors: | SHI Wei ZHU Hui-gang YAN Xiao-rong |
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| Affiliation: | 1.School of Public Health of Fudan University Former Shanghai University, Shanghai 200032, China |
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| Abstract: | Objective To study the mechanism of the hepatotoxicity of microcystion-UR.Methods MTT test and flow cytometry were applied in the research on the effects of microcystin-LR on the cell growth,cell cycle and apoptosis of primary cultured hepatocyte and Hela cell strain.Results Microcystic-LR can inhibit cell growth at very low dose and can promote cell proliferation at a relatively higher dose.Typical changes of apoptosis as well as and cell cycle block and synchronization at the G2/M-phase induced by mcirocystine-LR were observed.The results suggested that microcystin could affect hepatocyte cell cycles and induce cell proliferation as well as apoptosis.Similar but less distinct effect on Hela cell strain were detected.Conclusion It seemed that the special effects of microcystins on hepatocyte could be one of the mechanisms of hepatotoxicity of microcystins. |
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| Keywords: | MTT test flow cytometry microcystin cell growth cell cycle apoptosis |
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