环境激素烯菌酮引发小鼠前列腺癌细胞的毒性机制

摘要

To study the toxic mechanism of environmental hormone vinclozolin on mouse prostate cancer (RM-1) cells,3 groups experiments were designed: control group,vinclozolin-treated group,and addition of vitamin E to vinckozolin-treated group (experimental group).After 48 h,morphological changes of the cells were observed.Cell proliferation rate,makmdialdehyde (MDA) content and the ability to inhibit hydroxyl radical were determined as well as the activities of lactate dehydrogenase (LDH),Na+ -K+ -ATPase and Ca2+ -Mg2+ -ATPase.Compared with control group,the number of RM-1 adherent cells,cell proliferation rate,the ability to inhibit hydroxyl radical,Na+ -K+-ATPase activity and Ca2+ -Mg2+ -ATPase activity significantly decreased (p <0.05),while LDH activity and MDA content obviously increased (p <0.05) in vinclozolin-treated group.After addition of vitamin E,compared with vinclozolin-treated group,the number of adherent cells,cell proliferation rate,the ability to inhibit the hydroxyl radical,Na+ -K+ -ATPase activity and Ca2 +-Mg2 +-ATPase activity (p <0.05) significantly increased,while LDH activity and MDA content obviously decreased (p <0.05).It was indicated that vitamin E antagonized the oxidative stress of RM-1 cells treated with vinclozo-lin.Thus,the damage of cell membrane was relieved and the integrity and function of cells were maintained,preventing the escape of intraceDuiar LDH and the decreasing Na+ -K+ -ATPase activity and Ca2 + -Mg2+ -ATPase activity.As a result,the cell death and cell proliferation rate decreased.%为探讨环境激素烯菌酮引发小鼠前列腺癌(RM-1)细胞毒性机制,设计了3组实验,分别为对照组、烯菌酮染毒组(染毒组)和烯菌酮染毒后添加维生素E组(实验组),各组给药培养48 h后,观察细胞形态变化.检测细胞增殖活性、丙二醛(MDA)含量、抑制羟自由基能力、乳酸脱氢酶(LDH)活性、Na+ -K+ -ATP酶活性和Ca2+ -Mg2 -ATP酶活性.结果表明,与对照组相比,染毒组RM-1细胞圆缩脱落明显,贴壁细胞减少;细胞增殖率、抑制羟自由基能力、Na+ -K+ -ATP酶活性和Ca2+ -Mg2+-ATP酶活性明显降低(p＜0.05),LDH活性和MDA含量显著升高(p＜0.05).与染毒组相比,染毒后添加维生素E,圆缩脱落细胞减少,而梭形贴壁细胞明显增加;细胞增殖率、抑制羟自由基能力、Na+ -K+ -ATP酶活性和Ca2+-Mg2+ -ATP酶活性显著升高(p＜0.05),LDH活性和MDA含量明显下降(p＜0.05).这表明维生素E可能通过其抗氧化性拮抗了烯菌酮引发的氧化应激,缓解了细胞膜的损伤,维持了细胞膜的完整性和膜蛋白的功能,防止了细胞内LDH外逸、Na+ -K+ -ATP酶和Ca+ -Mg2+ -ATP酶活性的下降,从而逆转了烯菌酮引发的细胞死亡和增殖率的下降.