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首页> 外文期刊>International Journal of Environmental Research and Public Health >DNA Damage, Cell Cycle Arrest, and Apoptosis Induction Caused by Lead in Human Leukemia Cells
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DNA Damage, Cell Cycle Arrest, and Apoptosis Induction Caused by Lead in Human Leukemia Cells

机译：铅引起的人类白血病细胞DNA损伤，细胞周期阻滞和凋亡诱导

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In recent years, the industrial use of lead has been significantly reduced from paints and ceramic products, caulking, and pipe solder. Despite this progress, lead exposure continues to be a significant public health concern. The main goal of this research was to determine the in vitro mechanisms of lead nitrate [Pb(NO3)2] to induce DNA damage, apoptosis, and cell cycle arrest in human leukemia (HL-60) cells. To reach our goal, HL-60 cells were treated with different concentrations of Pb(NO3)2 for 24 h. Live cells and necrotic death cells were measured by the propidium idiode (PI) assay using the cellometer vision. Cell apoptosis was measured by the flow cytometry and DNA laddering. Cell cycle analysis was evaluated by the flow cytometry. The result of the PI demonstrated a significant (p < 0.05) increase of necrotic cell death in Pb(NO3)2-treated cells, indicative of membrane rupture by Pb(NO3)2 compared to the control. Data generated from the comet assay indicated a concentration-dependent increase in DNA damage, showing a significant increase (p < 0.05) in comet tail-length and percentages of DNA cleavage. Data generated from the flow cytometry assessment indicated that Pb(NO3)2 exposure significantly (p < 0.05) increased the proportion of caspase-3 positive cells (apoptotic cells) compared to the control. The flow cytometry assessment also indicated Pb(NO3)2 exposure caused cell cycle arrest at the G0/G1 checkpoint. The result of DNA laddering assay showed presence of DNA smear in the agarose gel with little presence of DNA fragments in the treated cells compared to the control. In summary, Pb(NO3)2 inhibits HL-60 cells proliferation by not only inducing DNA damage and cell cycle arrest at the G0/G1 checkpoint but also triggering the apoptosis through caspase-3 activation and nucleosomal DNA fragmentation accompanied by secondary necrosis. We believe that our study provides a new insight into the mechanisms of Pb(NO3)2 exposure and its associated adverse health effects.
机译：近年来，油漆和陶瓷产品，嵌缝和管道焊料中铅的工业使用已大大减少。尽管取得了这一进展，但铅暴露仍然是一个重大的公共卫生问题。这项研究的主要目的是确定硝酸铅[Pb（NO3）2]诱导人白血病（HL-60）细胞DNA损伤，细胞凋亡和细胞周期停滞的体外机制。为了达到我们的目标，用不同浓度的Pb（NO3）2处理HL-60细胞24小时。活细胞和坏死性死亡细胞是使用细胞计数仪通过丙二叉（PI）测定法测量的。通过流式细胞仪和DNA梯化法测量细胞凋亡。通过流式细胞术评估细胞周期分析。 PI的结果表明，用Pb（NO3）2处理的细胞中坏死细胞死亡显着增加（p <0.05），这表明与对照相比，Pb（NO3）2引起的膜破裂。彗星试验产生的数据表明，DNA损伤的浓度依赖性增加，表明彗星尾巴长度和DNA切割百分比显着增加（p <0.05）。流式细胞仪评估产生的数据表明，与对照相比，Pb（NO3）2暴露显着（p <0.05）增加了caspase-3阳性细胞（凋亡细胞）的比例。流式细胞仪评估还表明，Pb（NO3）2暴露导致细胞周期停滞在G0 / G1检查点。 DNA阶梯分析的结果表明，与对照相比，琼脂糖凝胶中存在DNA涂片，而处理过的细胞中几乎没有DNA片段存在。总之，Pb（NO3）2不仅通过在G0 / G1检查点诱导DNA损伤和细胞周期停滞，而且通过caspase-3活化和核小体DNA断裂并伴有继发性坏死来诱导细胞凋亡，从而抑制HL-60细胞增殖。我们相信我们的研究为Pb（NO3）2暴露及其相关的不良健康影响机制提供了新的见识。

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