Laboratory of Biochemistry, School of Medicine, University of Patras, 26504 Patras, Greece.
Aquat Toxicol. 2013 Jun 15;134-135:23-33. doi: 10.1016/j.aquatox.2013.02.014. Epub 2013 Mar 13.
Mercury is an element naturally occurring in the biosphere, but is also released into the environment by human activities, such as mining, smelting, and industrial discharge. Mercury is a biologically harmful element and any exposure of living organisms mainly due to contamination, can cause severe or even lethal side effects. In every form detected, elemental, inorganic, or organic, mercury exhibits toxicity associated with induced oxidative stress. Although the genotoxicity of mercury has been well demonstrated in mussels, little is known about its toxic effects on the translational machinery at the molecular level. To investigate possible effects, we exposed the common mussel Mytilus galloprovincialis in seawater supplemented by 30 μg/L Hg²⁺ for 15 days. We observed that Hg²⁺ was significantly accumulated in the digestive glands of mussels, reaching a level around 80 μg/g tissue (dry weight) at the 15th day of exposure. Exposure of mussels to Hg²⁺ resulted in failure of redox homeostasis, as reflected on lipid peroxidation levels and superoxide dismutase activity in glands, and micronucleus frequency in gills. Extracts from digestive glands after 15-day exposure to Hg²⁺ exhibited decreased tRNA aminoacylation ability and, moreover, a 70% reduction in the ability of 40S ribosomal subunits to form the 48S initiation ribosomal complex. A similar reduction was detected in the ability of ribosomes to translocate peptidyl-tRNA from the A-site to the P-site, an observation coinciding with the notion that regulation of protein synthesis by Hg²⁺ mainly occurs at the initiation and elongation stages of translation. A-site binding, peptidyl transferase activity, and termination of peptide chain synthesis underwent less pronounced but measurable reductions, a finding which explains why poly(Phe)-synthesis in ribosomes isolated from exposed mussels is reduced by 70%. In conclusion, Hg²⁺ apart from being a genotoxic ion acts as a modulator of protein synthesis in mussels, an observation probably related with its ability to induce oxidative stress.
汞是生物圈中自然存在的一种元素,但也是人类活动如采矿、冶炼和工业排放释放到环境中的。汞是一种对生物有害的元素,任何生物体的暴露主要是由于污染,都会导致严重甚至致命的副作用。在检测到的所有形式中,元素态、无机态或有机态的汞都表现出与诱导氧化应激相关的毒性。虽然汞的遗传毒性在贻贝中得到了很好的证明,但对其在分子水平上对翻译机制的毒性影响知之甚少。为了研究可能的影响,我们将普通贻贝 Mytilus galloprovincialis 暴露在添加了 30μg/L Hg²⁺的海水中 15 天。我们观察到 Hg²⁺在贻贝的消化腺中显著积累,在暴露的第 15 天达到约 80μg/g 组织(干重)的水平。贻贝暴露于 Hg²⁺导致氧化还原稳态失效,这反映在腺中脂质过氧化水平和超氧化物歧化酶活性以及鳃中的微核频率上。暴露于 Hg²⁺ 15 天后消化腺的提取物显示出 tRNA 氨酰化能力下降,并且 40S 核糖体亚基形成 48S 起始核糖体复合物的能力下降了 70%。核糖体从 A 位到 P 位转移肽酰-tRNA 的能力也观察到类似的降低,这一观察结果与 Hg²⁺主要在翻译的起始和延伸阶段调节蛋白质合成的观点一致。A 位结合、肽基转移酶活性和肽链合成终止的降低幅度较小,但仍可测量,这一发现解释了为什么暴露贻贝中分离的核糖体上的多(Phe)合成减少了 70%。总之,Hg²⁺除了是一种遗传毒性离子外,还作为贻贝中蛋白质合成的调节剂,这一观察结果可能与其诱导氧化应激的能力有关。