Laboratory of Biochemistry, School of Medicine, University of Patras, 26504 Patras, Greece.
J Hazard Mater. 2013 Sep 15;260:263-71. doi: 10.1016/j.jhazmat.2013.05.031. Epub 2013 May 22.
The main purpose of this study was to investigate the impact of metal-mediated stress on the protein-synthesis pathway in mussels. To this end, mussels (Mytilus galloprovincialis) underwent a 15 days exposure to 100 μg/L Cu(2+) or Cd(2+). Both metals, in particular Cd(2+), accumulated in mussel digestive glands and generated a specific status of oxidative-stress. Exposure of mussels to each metal resulted in 40% decrease of the tRNA-aminoacylation efficiency, at the end of exposure. Cu(2+) also caused a progressive loss in the capability of 40S-ribosomal subunits to form 48S pre-initiation complex, which reached 34% of the control at the end of exposure. Other steps of translation underwent less pronounced, but measurable damages. Mussels exposed to Cd(2+) for 5 days presented a similar pattern of translational dysfunctions in digestive glands, but during the following days of exposure the ribosomal efficiency was gradually restored. Meanwhile, metallothionein levels significantly increased, suggesting that upon Cd(2+)-mediated stress the protein-synthesizing activity was reorganized both quantitatively and qualitatively. Conclusively, Cd(2+) and Cu(2+) affect translation at several levels. However, the pattern of translational responses differs, largely depending on the capability of each metal to affect cytotoxic pathways in the tissues, such as induction of antioxidant defense and specific repair mechanisms.
本研究的主要目的是探讨金属介导的应激对贻贝蛋白质合成途径的影响。为此,贻贝(Mytilus galloprovincialis)经历了 15 天 100μg/L Cu(2+)或 Cd(2+)暴露。两种金属,特别是 Cd(2+),在贻贝消化腺中积累并产生特定的氧化应激状态。暴露于每种金属最终导致 tRNA-氨酰化效率降低 40%。Cu(2+)还导致 40S 核糖体亚基形成 48S 起始前复合物的能力逐渐丧失,暴露结束时达到对照的 34%。其他翻译步骤受到的损害虽不明显,但仍可测量。暴露于 Cd(2+) 5 天的贻贝在消化腺中表现出类似的翻译功能障碍模式,但在随后的暴露天数中,核糖体效率逐渐恢复。同时,金属硫蛋白水平显著增加,表明在 Cd(2+)介导的应激下,蛋白质合成活性在数量和质量上都得到了重新组织。总之,Cd(2+)和 Cu(2+)在多个水平上影响翻译。然而,翻译反应的模式不同,这在很大程度上取决于每种金属影响组织细胞毒性途径的能力,如诱导抗氧化防御和特定修复机制。