Metallothionein blocks oxidative DNA damage induced by acute inorganic arsenic exposure.

Metallothionein blocks oxidative DNA damage induced by acute inorganic arsenic exposure.
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DOI:
10.1016/j.taap.2014.11.014
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发表时间:
2015-02-01
影响因子:
3.8
通讯作者:
Waalkes, Michael P.
Waalkes, Michael P.
中科院分区:
医学3区
文献类型:
--
作者:
Qu, Wei;Waalkes, Michael P.

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我们使用低表达 MT 的细胞(MT-I/II 双敲除胚胎细胞;称为 MT 无效细胞)和野生型 (WT) MT 感受态细胞,研究了金属硫蛋白 (MT) 蛋白如何影响砷诱导的氧化 DNA 损伤 (ODD)。砷(以 NaAsO2 形式)在 24 小时内对 WT 细胞的细胞致死作用(LC50 = 11.0 ± 1.3 µM;平均值 ± SEM)低于 MT 无效细胞(LC50 = 5.6 ± 1.2 µM)。 ODD通过免疫自旋捕获法测量。砷(1 或 5 µM;24 小时)在 WT 细胞中诱导的 ODD(分别为对照的 121% 和 141%)比 MT 无效细胞(202% 和 260%)少得多。在 WT 细胞中,砷导致 MT 表达(转录本和蛋白质)以及金属响应转录因子-1 (MTF-1) 的浓度依赖性增加,这是诱导 MT 基因所必需的。相比之下,MT 缺失细胞中检测不到基础 MT 水平,并且砷暴露不会改变基础 MT 水平。将MT-I转染至MT无效细胞中显着降低了砷诱导的ODD水平。在 WT 细胞中,转运基因 Abcc1 和 Abcc2 因砷而增加,但在 MT-null 细胞中则没有显示或显示出非常有限的增加。砷会导致 WT 和 MT-null 细胞中氧化应激防御基因 HO-1 和 GSTa2 的增加,但在 WT 细胞中水平要高得多。 WT 细胞似乎更擅长激活金属转运系统和氧化反应基因,尽管 MT 在这些反应中的作用尚不清楚。总体而言,MT 通过潜在地隔离清除氧化剂自由基和/或砷来防止 MT 感受态细胞中砷诱导的 ODD。
We studied how the protein metallothionein (MT) impacts arsenic-induced oxidative DNA damage (ODD) using cells that poorly express MT (MT-I/II double knockout embryonic cells; called MT-null cells) and wild-type (WT) MT competent cells. Arsenic (as NaAsO2) was less cytolethal over 24 h in WT cells (LC50 = 11.0 ± 1.3 µM; mean ± SEM) than in MT-null cells (LC50 = 5.6 ± 1.2 µM). ODD was measured by the immuno-spin trapping method. Arsenic (1 or 5 µM; 24 h) induced much less ODD in WT cells (121% and 141% of control, respectively) than in MT-null cells (202% and 260%). In WT cells arsenic caused concentration-dependent increases in MT expression (transcript and protein), and in the metal-responsive transcription factor-1 (MTF-1), which is required to induce the MT gene. In contrast, basal MT levels were not detectable in MT-null cells and unaltered by arsenic exposure. Transfection of MT-I into the MT-null cells markedly reduced arsenic-induced ODD levels. The transport genes, Abcc1 and Abcc2 were increased by arsenic in WT cells but either showed no or very limited increases in MT-null cells. Arsenic caused increases in oxidant stress defense genes HO-1 and GSTa2 in both WT and MT-null cells, but to much higher levels in WT cells. WT cells appear more adept at activating metal transport systems and oxidant response genes, although the role of MT in these responses is unclear. Overall, MT protects against arsenic-induced ODD in MT competent cells by potentially sequestration of scavenging oxidant radicals and/or arsenic.
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