Immunology and Microbiology Laboratory, Department of Human Physiology with Community Health, Vidyasagar University, Midnapore 721 102, West Bengal, India.
Nano materials Laboratory, Department of Chemistry, Indian Institute of Technology, Kharagpur, West Bengal, India.
Chem Biol Interact. 2015 Jan 25;226:58-71. doi: 10.1016/j.cbi.2014.11.016. Epub 2014 Nov 28.
The aim of this study was to find out the intracellular signaling transduction pathways involved in cobalt oxide nanoparticles (CoO NPs) mediated oxidative stress in vitro and in vivo system. Cobalt oxide nanoparticles released excess Co++ ions which could activated the NADPH oxidase and helps in generating the reactive oxygen species (ROS). Our results showed that CoO NPs elicited a significant (p<0.05) amount of ROS in lymphocytes. In vitro pretreatment with N-acetylene cystine had a protective role on lymphocytes death induced by CoO NPs. In vitro and in vivo results showed the elevated level of TNF-α after CoO NPs treatment. This TNF-α phosphorylated the p38 mitogen-activated protein kinase followed by activation of caspase 8 and caspase 3 which could induce cell death. This study showed that CoO NPs induced oxidative stress and activated the signaling pathway of TNF-α-caspase-8-p38-caspase-3 to primary immune cells. This study suggested that bare CoO NPs are a toxic for primary human immune cells that deals directly with human health. Surface modification or surface functionalization may open the gateway for further use of CoO NPs in different industrial use or in biomedical sciences.
本研究旨在探讨体外和体内系统中氧化应激钴氧化物纳米颗粒（CoO NPs）介导的细胞内信号转导途径。钴氧化物纳米颗粒释放过量的 Co++离子，激活 NADPH 氧化酶，生成活性氧（ROS）。我们的结果表明，CoO NPs 可引起淋巴细胞中显著（p<0.05）数量的 ROS。体外预先用 N-乙酰半胱氨酸处理可对 CoO NPs 诱导的淋巴细胞死亡起保护作用。体外和体内结果显示，CoO NPs 处理后 TNF-α 水平升高。该 TNF-α 磷酸化丝裂原活化蛋白激酶 p38，随后激活 caspase 8 和 caspase 3，诱导细胞死亡。本研究表明，CoO NPs 可诱导氧化应激并激活 TNF-α-caspase-8-p38-caspase-3 信号通路，影响原代免疫细胞。该研究表明，裸露的 CoO NPs 对直接接触人体健康的原代人免疫细胞具有毒性。表面改性或表面功能化可能为 CoO NPs 在不同工业用途或生物医学科学中的进一步应用开辟道路。
