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首页> 外文期刊>RSC Advances >Cadmium induced apoptosis in mouse primary hepatocytes: the role of oxidative stress-mediated ERK pathway activation and the involvement of histone H3 phosphorylation
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Cadmium induced apoptosis in mouse primary hepatocytes: the role of oxidative stress-mediated ERK pathway activation and the involvement of histone H3 phosphorylation

机译：小鼠初级肝细胞中镉诱导的细胞凋亡：氧化应激介导的ERK途径激活的作用及组蛋白H3磷酸化的累积

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摘要

Cadmium can disturb the intracellular redox state and generate oxidative stress, leading to a variety of diseases. A number of studies have reported that oxidative stress and activation of mitogen-activated protein kinase pathways contributes to the induction or inhibition of apoptosis, depending on the types of cell lines and stimulus. However, the role of oxidative stress and the activation of extracellular signal-regulated kinase (ERK) signaling pathways in the apoptosis of cadmium-treated primary hepatocytes and its underlying mechanism still remain unclear. The present study clearly confirms the important role of oxidative stress in the time-delayed effects of cadmium-induced apoptosis. Rather than direct induction by cadmium, cadmium decreased cell viability by causing oxidative stress mediated-apoptosis after 24 h exposure. This was verified by the persistent elevation of excessive reactive oxygen species and DNA oxidative damage, the decrease in glutathione level and the protection of N-acetyl-L-cysteine (NAC). Furthermore, NAC and PD98059 prevented apoptosis, caspase-3 activation and histone H3 phosphorylation. Also, NAC suppressed Cd-induced activation of the ERK pathway. These results demonstrated that oxidative stress-regulated downstream ERK pathway activation plays a pivotal role in Cd-induced apoptosis of primary hepatocytes. The present study also indicates for the first time that Cd-induced histone H3 phosphorylation is closely associated with activation of the ERK pathway and is involved in oxidative stress-mediated DNA damage and cell death. These results will contribute to a better understanding of the cellular mechanisms of cadmium toxicity and its effects on human health.
机译：镉可以干扰细胞内氧化还原状态并产生氧化应激，导致各种疾病。许多研究报道说，氧化应激和丝裂剂活化蛋白激酶途径的激活有助于诱导或抑制细胞凋亡，这取决于细胞系和刺激的类型。然而，氧化应激的作用和细胞外信号调节激酶（ERK）信号传导途径在镉处理的原发性肝细胞的凋亡中及其下面的机制仍然不清楚。本研究清楚地证实氧化应激在镉诱导的细胞凋亡的时间延迟作用中的重要作用。通过在24小时暴露后引起氧化应激介导的凋亡，镉而不是直接诱导镉，镉降低了细胞活力。通过过度反应性氧物质和DNA氧化损伤的持续升高，这是验证的，降低谷胱甘肽水平和N-乙酰-1-半胱氨酸（NAc）的保护。此外，NAC和PD98059预防细胞凋亡，Caspase-3活化和组蛋白H3磷酸化。此外，NAC抑制了ERK途径的CD诱导的激活。这些结果表明，氧化应激调节的下游ERK途径活化在致肝细胞的CD诱导的凋亡中起着关键作用。本研究还表明，第一次表明CD诱导的组蛋白H3磷酸化与ERK途径的激活密切相关，并且参与氧化应激介导的DNA损伤和细胞死亡。这些结果将有助于更好地理解镉毒性的细胞机制及其对人体健康的影响。

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  • 来源
    《RSC Advances》 |2015年第40期|共9页
  • 作者

    Wang Jing; Hao Minglu; Liu Chunguang; Liu Rutao;

  • 作者单位

    Shandong Univ Sch Environm Sci &

    Engn China Amer CRC Environm &

    Hlth Jinan 250100 Shandong Peoples R China;

    Shandong Univ Sch Environm Sci &

    Engn China Amer CRC Environm &

    Hlth Jinan 250100 Shandong Peoples R China;

    Shandong Univ Sch Environm Sci &

    Engn China Amer CRC Environm &

    Hlth Jinan 250100 Shandong Peoples R China;

    Shandong Univ Sch Environm Sci &

    Engn China Amer CRC Environm &

    Hlth Jinan 250100 Shandong Peoples R China;

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