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首页> 外文期刊>Aquatic Toxicology >Short-term metallothionein inductions in the edible cockle Cerastoderma edule after cadmium or mercury exposure: discrepancy between mRNA and protein responses.
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Short-term metallothionein inductions in the edible cockle Cerastoderma edule after cadmium or mercury exposure: discrepancy between mRNA and protein responses.

机译：镉或汞暴露后可食用鸟蛤皮中的短期金属硫蛋白诱导：mRNA和蛋白质反应之间的差异。

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摘要

Metallothioneins (MT) are essential metal binding proteins involved in metal homeostasis and detoxification in living organisms. Numerous studies have focused on MT response to metal exposure and showed an important variability according to species, metal, concentration and time of exposure. In this study, the expression of one isoform of MT gene (Cemt1) and associated MT protein synthesis were determined after 1, 3, 9, 24, 72 and 168 h of cadmium (Cd) or mercury (Hg) exposures in gills of the cockle Cerastoderma edule. This experiment, carried out in laboratory conditions, revealed that in Cd-exposed cockles, induction of Cemt1 is time-dependent following a "pulse-scheme" with significant upregulation at 24 h and 168 h intersected by time point (72 h) with significant downregulation. MT protein concentration increases with time in gills of exposed cockles in relation with the progressive accumulation of Cd in soluble fraction. On contrary, Hg exposure does not lead to any induction of Cemt1 mRNA expression or MT protein synthesis compared to control, despite a higher accumulation of this metal in gills of cockles compared to Cd. The localization of Hg (85-90%) is in insoluble fraction, whereas MT was located in the cytoplasm of cells. This gives us a first clue to understand the inability of Hg to activate MT synthesis. However, other biochemical processes probably occur in gills of C. edule since the remaining soluble fraction of Hg exceeds MT sequestration ability. Finally, since one of the first main targets of metal toxicity in cells was the mitochondria, some genes involved in mitochondria metabolism were also analyzed in order to assess potential differences in cellular damages between two metal exposures. Indeed, until T168, no impact on mitochondrial genes was shown following Hg exposure, despite the complete lack of MT response. This result indicated the presence of other effective cellular ligands which sequester the cytosolic fraction of this metal and consequently inhibit metal reactivity. Such competition mechanisms with other cytosolic ligands more sensitive to Hg were particularly argued in the discussion.
机译：金属硫蛋白（MT）是参与金属生物体内金属稳态和排毒的必需金属结合蛋白。许多研究集中于MT对金属暴露的反应，并显示出根据物种，金属，浓度和暴露时间的重要差异。在这项研究中，在镉（Cd）或汞（Cd）1、3、9、24、72和168小时后确定了MT基因的一种同工型（ Cemt1 ）的表达和相关的MT蛋白合成。 Hg）暴露于蛤le 皮疹皮肤的g中。该实验是在实验室条件下进行的，结果表明，在暴露于镉的鸟蛤中， Cemt1 的诱导是“时间依赖性的”，这是由于“脉冲方案”在时间相交的24 h和168 h有明显的上调点（72小时）明显下调。相对于镉在可溶性级分中的逐步积累，暴露的蛤cock中MT蛋白的浓度随时间增加。相反，与对照组相比，汞暴露不会导致 Cemt1 mRNA表达或MT蛋白合成的任何诱导，尽管与Cd相比，这种金属在鸟蛤g中的积累更高。 Hg（85-90％）的定位是不溶级分，而MT位于细胞的细胞质中。这为我们提供了了解汞不能激活MT合成的第一个线索。但是，其他生化过程可能在i g中发生。因为汞的剩余可溶性部分超过了MT的螯合能力。最后，由于细胞中金属毒性的第一个主要靶标是线粒体，因此还分析了一些参与线粒体代谢的基因，以评估两次金属暴露之间细胞损伤的潜在差异。实际上，直到 T 168 为止，尽管完全没有MT反应，但暴露于Hg后对线粒体基因没有影响。该结果表明存在其他有效的细胞配体，其螯合该金属的胞质部分并因此抑制金属反应性。在讨论中特别提出了与其他对Hg更加敏感的胞质配体的竞争机制。

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