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首页> 外文期刊>Journal of biochemical and molecular toxicology >Cadmium- and chromium-induced oxidative stress, DNA damage, and apoptotic cell death in cultured human chronic myelogenous leukemic K562 cells, promyelocytic leukemic HL-60 cells, and normal human peripheral blood mononuclear cells.
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Cadmium- and chromium-induced oxidative stress, DNA damage, and apoptotic cell death in cultured human chronic myelogenous leukemic K562 cells, promyelocytic leukemic HL-60 cells, and normal human peripheral blood mononuclear cells.

机译：镉和铬诱导的氧化胁迫，DNA损伤和培养的人慢性髓性白血病K562细胞，早幼细胞白血病HL-60细胞和正常人外周血单核细胞中的凋亡细胞死亡。

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摘要

Sodium dichromate [Cr(VI)] and cadmium chloride [Cd(II)] are both cytotoxic and mutagenic. This study examined the toxic and apoptotic potentials of these two cations on three cell types in vitro, namely, human chronic myelogenous leukemic (CML) K562 cells, promyelocytic leukemic HL-60 cells, and normal human peripheral blood mononuclear cells. The cells were incubated with 0-100 microM concentrations of the two cations for 0, 24, or 48 hours at 37 degrees C. Both Cr(VI) and Cd(II) induced changes in intracellular oxidized states of cells, which were detected using laser scanning confocal microscopy. Cell cycle modulation and apoptosis of the K562 cells by Cr(VI) and Cd(II) were determined by flow cytometry. Significant decreases in the G2/M phase were observed in the Cr(VI) and Cd(II) treated CML cells compared with untreated cells. At 12.5 microM, Cr(VI) induced greater apoptosis in K562 cells as compared with Cd(II). In the K562 cells, 2.2- and 3.0-fold increases in DNA fragmentation were observed following incubation with 12.5 and 25 microM Cr(VI), respectively, and 1.2- and 1.7-fold increases in DNA fragmentation were observed with Cd(II). Furthermore, approximately 2.7- and 4.9-fold increases in cytochrome c reduction were observed following incubation with 12.5 and 25 microM Cr(VI), respectively, and 1.6- and 3.3-fold increases in cytochrome c reduction were observed with Cd(II), demonstrating enhanced production of superoxide anion. Approximately 3.1 to 6-fold increases in hydroxyl radical production were observed following incubation of the K562 cells with these cations at 12.5 and 25 microM concentrations. These results in K562 cells were compared with promyelocytic leukemic HL-60 cells and normal human peripheral blood mononuclear cells. More pronounced effects were observed on K562 and HL-60 cells, and much lesser effects were observed on normal human peripheral blood mononuclear cells. The results demonstrate that both cations are toxic, producing oxidative tissue damage and apoptosis. Furthermore, more drastic effects were observed on K562 and HL-60 cells as compared with normal human peripheral blood mononuclear cells.
机译：二甲磺酸钠[Cr（VI）]和氯化镉[CD（II）]是细胞毒性和诱变的。本研究在体外，即人慢性髓性白血病（CML）K562细胞，幼胞菌白血病HL-60细胞和正常的人外周血单核细胞中，研究了这两个阳离子的毒性和凋亡潜力。将细胞与0,24或48小时的0-100微米浓度在37℃下孵育.Cr（VI）和CD（II）诱导的细胞内氧化态的变化，其使用激光扫描共聚焦显微镜。通过流式细胞术测定Cr（VI）和Cd（II）的细胞周期调制和K562细胞的凋亡。与未处理的细胞相比，在Cr（VI）和CD（II）处理的CML细胞中，在Cr（VI）和CD（II）处理的CML细胞中观察到G2 / M相的显着降低。在12.5微米，与CD（II）相比，Cr（VI）在K562细胞中诱导更高的细胞凋亡。在K562细胞中，在与12.5和25微米Cr（VI）孵育后观察到DNA片段化的2.2-和3.0倍的增加，用CD（II）观察到DNA碎片中的1.2-和1.7倍。此外，在与12.5和25微米Cr（VI）一起孵育后观察到细胞色素C还原的约2.7-和4.9倍，并且用CD（II）观察到细胞色素C的1.6-和3.3倍的增加，展示增强的超氧化物阴离子的生产。在将K562细胞与12.5和25微米浓度下温育后，观察到在K562细胞的温育后观察到羟基自由基的增加约3.1至6倍。将这些结果与高幼粒细胞白血病HL-60细胞和正常的人外周血单核细胞进行比较。在K562和HL-60细胞上观察到更明显的效果，在正常人外周血单核细胞上观察到更大的效果。结果表明，两个阳离子都有毒，产生氧化组织损伤和凋亡。此外，与正常人外周血单核细胞相比，在K562和HL-60细胞上观察到更激烈的效果。

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