Cadmium-induced oxidative damages in the human BJAB cells correlate with changes in intracellular trace elements levels and zinc transporters expression.
Cadmium-induced oxidative damages in the human BJAB cells correlate with changes in intracellular trace elements levels and zinc transporters expression.
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DOI：
10.1016/j.tiv.2016.09.014
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发表时间：
2016-12
期刊：
影响因子：
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通讯作者：
S. Nemmiche;P. Guiraud
中科院分区：
文献类型：
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作者：
S. Nemmiche;P. Guiraud
镉（Cd）是一种毒性很强的重金属，是一种广泛存在的环境污染物。其通过过渡金属通道的细胞交通有助于毒性机制。锌（Zn）的动态平衡是复杂的，涉及锌进口商（Zip）和锌出口商（ZnT）。细胞信号转导通路受锌和细胞氧化还原状态的影响。本研究旨在探讨人淋巴细胞B细胞系BJAB中Cd的积累及其促进氧化应激和不良反应的能力是否可能与锌转运体和金属硫蛋白mRNA表达模式的改变有关。cdcl2浓度分别为0.91、1.83、3.66和7.33 μg/ml，浓度为5、10、20和40 μM，暴露24 h后，BJAB细胞活力明显降低，DNA损伤呈剂量依赖性增加。Cd还诱导BJAB细胞中8-羟基-2 ' -脱氧鸟苷加合物的形成，并增加MTF1的表达。在我们分析的七个转运蛋白中，我们观察到相对基因表达对Cd暴露的有趣反应。Cd暴露使DMT1表达增加，ZnT1表达上调。而T钙通道α 1g亚基未被检测到。锌转运体参与镉细胞代谢和诱导氧化应激的研究表明，锌转运体参与镉细胞代谢和氧化应激。
Cadmium (Cd), a potent toxic heavy metal, is a widespread environmental contaminant. Its cellular traffic via pathways dedicated to transition metals contributes to the toxicity mechanisms. Zinc (Zn) homeostasis is complex, involving both zinc importers (Zip) and zinc exporters (ZnT). Cellular signal transduction pathways are influenced by Zn and redox status of the cell. The aim of the present study is to examine if the accumulation of Cd in the human lymphocyte B cell line BJAB and its capacity to promote oxidative stress and adverse effects could result from changes in the mRNA expression pattern of Zn transporters and metallothioneins. Cells were exposed to 5, 10, 20 and 40 μM of CdCl2equivalent to 0.91, 1.83, 3.66 and 7.33 μg/ml respectively, for 24 h. Cd significantly reduced the viability of BJAB cells and induced a dose-dependent increase in DNA damage. Cd also induced the formation of 8-hydroxy-2′-deoxyguanosine adducts and augmented MTF1 expression in BJAB cells. We observed interesting responses in relative gene expression to Cd exposure among the seven transporters we analyzed. Cd exposure increased the expression of DMT1 and caused an up-regulation of ZnT1. However, the T calcium channel alpha1G subunit could not be detected. A change in expression of ZnTs and Zips in response to Cd exposure emphasizes the involvement of Zn transporters in Cd cellular metabolism and induced oxidative stress.