Mercury chloride (HgCl2) is a chemical pollutant widely found in the environment. This form of mercury is able to promote several damages to the Central Nervous System (CNS), however the effects of HgCl2 on the spinal cord, an important pathway for the communication between the CNS and the periphery, are still poorly understood. The aim of this work was to investigate the effects of HgCl2 exposure on spinal cord of adult rats. For this, animals were exposed to a dose of 0.375 mg/kg/day, for 45 days. Then, they were euthanized, the spinal cord collected and we investigated the mercury concentrations in medullary parenchyma and the effects on oxidative biochemistry, proteomic profile and tissue structures. Our results showed that exposure to this metal promoted increased levels of Hg in the spinal cord, impaired oxidative biochemistry by triggering oxidative stress, mudulated antioxidant system proteins, energy metabolism and myelin structure; as well as caused disruption in the myelin sheath and reduction in neuronal density. Despite the low dose, we conclude that prolonged exposure to HgCl2 triggers biochemical changes and modulates the expression of several proteins, resulting in damage to the myelin sheath and reduced neuronal density in the spinal cord.

中文翻译：

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成年大鼠长期接触无机汞后脊髓神经变性：与神经元密度降低相关的超微结构，蛋白质组学和生化损伤。

氯化汞（HgCl2）是在环境中广泛发现的化学污染物。这种形式的汞能够促进对中枢神经系统（CNS）的多种损害，但是，人们仍然很少了解HgCl2对脊髓的影响，而脊髓是CNS与周围环境之间进行交流的重要途径。这项工作的目的是调查HgCl2暴露对成年大鼠脊髓的影响。为此，将动物暴露于0.375 mg / kg /天的剂量下45天。然后，将他们安乐死，收集脊髓，我们研究了髓实质中的汞浓度以及对氧化生物化学，蛋白质组学特征和组织结构的影响。我们的研究结果表明，接触这种金属可促进脊髓中Hg含量的增加，通过触发氧化应激，抗氧化系统蛋白泥化，能量代谢和髓磷脂结构破坏氧化生物化学；并导致髓鞘破裂和神经元密度降低。尽管剂量很低，但我们得出的结论是，长时间暴露于HgCl2会触发生化变化并调节几种蛋白质的表达，从而导致髓鞘受损和脊髓神经元密度降低。