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成年大鼠低剂量甲基汞暴露会导致氧化应激、运动皮层神经退行性变,并导致运动技能受损。

Low doses of methylmercury exposure during adulthood in rats display oxidative stress, neurodegeneration in the motor cortex and lead to impairment of motor skills.

机构信息

Laboratory of Functional and Structural Biology, Institute of Biological Sciences, Federal University of Pará, Belém, PA, Brazil.

Laboratory of Ecotoxicology, Institute of Biological Sciences, Federal University of Pará, Belém, PA, Brazil.

出版信息

J Trace Elem Med Biol. 2019 Jan;51:19-27. doi: 10.1016/j.jtemb.2018.09.004. Epub 2018 Sep 11.

DOI:10.1016/j.jtemb.2018.09.004
PMID:30466930
Abstract

Despite the vast distribution among tissues, the central nervous system (CNS) represents the main target of methylmercury (MeHg) toxicity. However, few studies have evaluated the effects of MeHg exposure on the CNS at equivalent doses to human environmental exposure. In our study, we evaluated the motor cortex, an important area of motor control, in adult rats chronically exposed to MeHg in a concentration equivalent to those found in fish-eating populations exposed to mercury (Hg). The parameters evaluated were total Hg accumulation, oxidative stress, tissue damage, and behavioral assessment in functional actions that involved this cortical region. Our results show in exposed animals a significantly greater level of Hg in the motor cortex; increase of nitrite levels and lipid peroxidation, associated with decreased antioxidant capacity against peroxyl radicals; reduction of neuronal and astrocyte density; and poor coordination and motor learning impairment. Our data showed that chronic exposure at low doses to MeHg is capable of promoting damages to the motor cortex of adult animals, with changes in oxidative biochemistry misbalance, neurodegeneration, and motor function impairment.

摘要

尽管甲基汞(MeHg)在组织中广泛分布,但中枢神经系统(CNS)是其毒性的主要靶标。然而,很少有研究以相当于人类环境暴露的剂量评估 MeHg 暴露对中枢神经系统的影响。在我们的研究中,我们评估了成年大鼠的运动皮层,这是运动控制的一个重要区域,这些大鼠长期暴露于与食用受汞(Hg)污染鱼类的人群中相同浓度的 MeHg 中。评估的参数包括总汞积累、氧化应激、组织损伤以及涉及该皮质区域的功能动作的行为评估。我们的结果表明,暴露组动物的运动皮层中 Hg 含量显著增加;亚硝酸盐水平和脂质过氧化增加,同时抗氧化能力对过氧自由基降低;神经元和星形胶质细胞密度减少;协调能力差,运动学习能力受损。我们的数据表明,慢性低剂量 MeHg 暴露能够导致成年动物运动皮层损伤,导致氧化生物化学失衡、神经退行性变和运动功能障碍。

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