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成年小鼠经口腔暴露于甲基汞导致的运动障碍。

Motor impairment induced by oral exposure to methylmercury in adult mice.

机构信息

Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.

出版信息

Environ Toxicol Pharmacol. 2005 Jan;19(1):169-75. doi: 10.1016/j.etap.2004.07.004.

Abstract

The effects of oral exposure to methylmercury chloride (MeHg) on locomotor control and activity in adult mice were investigated in the present study. MeHg was diluted in drinking water (0, 20 and 40mg/L - as methylmercury chloride) and locomotion (spontaneous locomotor activity) and motor impairment tests (beam walking, footprint and clasping) were performed at 7, 14 and 21 days after the beginning of the treatment. MeHg exposure caused a significant decrease in spontaneous locomotor activity and this effect was dose- and time-dependent. Significant dose- and duration-dependent increases in beam walking latency were observed following chronic MeHg exposure. Furthermore, dose- and duration-dependent locomotor deficits on footprint coordination were also observed. Taken together, these results show that MeHg-induced impairment on locomotor activity is not limited to exposures that take place during neural development. We discuss the possible relationship between our findings and the similar clinical signs observed in adult humans exposed to MeHg.

摘要

本研究探讨了经口摄入氯化甲基汞(MeHg)对成年小鼠运动控制和活动的影响。MeHg 被稀释在饮用水中(0、20 和 40mg/L-作为氯化甲基汞),并在治疗开始后 7、14 和 21 天进行运动(自发运动活动)和运动障碍测试(走棒、足迹和抓握)。MeHg 暴露导致自发运动活动显著减少,这种效应呈剂量和时间依赖性。慢性 MeHg 暴露后,走棒潜伏期显著增加,呈剂量和时间依赖性。此外,足迹协调运动障碍也呈现剂量和时间依赖性。综上所述,这些结果表明,MeHg 引起的运动活动障碍不仅限于在神经发育过程中进行的暴露。我们讨论了我们的发现与在成人中观察到的类似临床症状之间的可能关系。

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