Christensen M, Mogensen S C, Rungby J
Department of Neurobiology, Institute of Anatomy, Aarhus C, Denmark.
Arch Toxicol. 1988;62(6):440-6. doi: 10.1007/BF00288347.
The effects of mercuric chloride on cell survival, phagocytosis and cell migration were examined in cultured mouse peritoneal macrophages, and the accumulation of mercuric chloride in the cells was visualized by autometallography and evaluated by light and electron microscopy. Macrophages exposed to mercury concentrations from 1.25 microM to 10 microM mercuric chloride showed a concentration- and time-dependent increase in mercuric chloride accumulation, while cells exposed to 20 microM and 40 microM mercury showed an inverse relationship between mercury concentration and the accumulation of mercury. Mercury concentrations above these levels caused cell necrosis. Electron microscopy revealed that mercury was located primarily within lysosomes but also in the nucleus and cytoplasm. Mercury increased the death rate of macrophages in a concentration-dependent manner when cells were treated with mercury concentrations not causing cell necrosis. Further, we found that mercury clearly impaired macrophage random migration and possibly the capability for phagocytosis.
在培养的小鼠腹腔巨噬细胞中检测了氯化汞对细胞存活、吞噬作用和细胞迁移的影响,并通过自动金属显影法观察细胞中氯化汞的积累情况,同时利用光学显微镜和电子显微镜进行评估。暴露于浓度为1.25微摩尔至10微摩尔氯化汞的巨噬细胞,其氯化汞积累呈浓度和时间依赖性增加,而暴露于20微摩尔和40微摩尔汞的细胞,汞浓度与汞积累呈负相关。高于这些水平的汞浓度会导致细胞坏死。电子显微镜显示,汞主要位于溶酶体内,但也存在于细胞核和细胞质中。当用不会导致细胞坏死的汞浓度处理细胞时,汞以浓度依赖性方式增加巨噬细胞的死亡率。此外,我们发现汞明显损害巨噬细胞的随机迁移,可能还损害其吞噬能力。