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汞暴露大鼠的痛觉迟钝和恢复。

Hypoalgesia and recovery in methylmercury-exposed rats.

机构信息

Department of Environmental Health, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences.

Department of Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science.

出版信息

J Toxicol Sci. 2021;46(6):303-309. doi: 10.2131/jts.46.303.


DOI:10.2131/jts.46.303
PMID:34078837
Abstract

Methylmercury (MeHg), the causal substrate in Minamata disease, can lead to severe and chronic neurological disorders. The main symptom of Minamata disease is sensory impairment in the four extremities; however, the sensitivity of individual sensory modalities to MeHg has not been investigated extensively. In the present study, we performed stimulus-response behavioral experiments in MeHg-exposed rats to compare the sensitivities to pain, heat, cold, and mechanical sensations. MeHg (6.7 mg/kg/day) was orally administered to 9-week-old Wistar rats for 5 days and discontinued for 2 days, then administered daily for another 5 days. The four behavioral experiments were performed daily on each rat from the beginning of MeHg treatment for 68 days. The pain sensation decreased significantly from day 11 onwards, but recovered to control levels on day 48. Other sensory modalities were not affected by MeHg exposure. These findings suggest that the pain sensation is the sensory modality most susceptive to MeHg toxicity and that this sensitivity is reversible following discontinuation of the exposure.

摘要

甲基汞(MeHg)是水俣病的致病底物,可导致严重和慢性的神经障碍。水俣病的主要症状是四肢感觉障碍;然而,MeHg 对不同感觉模态的敏感性尚未得到广泛研究。在本研究中,我们在 MeHg 暴露的大鼠中进行了刺激-反应行为实验,以比较对疼痛、热、冷和机械感觉的敏感性。将 MeHg(6.7mg/kg/天)以口服方式给予 9 周龄 Wistar 大鼠,连续给药 5 天,然后停药 2 天,再连续给药 5 天。从 MeHg 处理的第一天开始,每天对每只大鼠进行四项行为实验,共进行 68 天。疼痛感觉从第 11 天开始显著降低,但在第 48 天恢复到对照水平。其他感觉模态不受 MeHg 暴露的影响。这些发现表明,疼痛感觉是对 MeHg 毒性最敏感的感觉模态,并且在停止暴露后这种敏感性是可逆的。

相似文献

[1]
Hypoalgesia and recovery in methylmercury-exposed rats.

J Toxicol Sci. 2021

[2]
[Methylmercury causes diffuse damage to the somatosensory cortex: how to diagnose Minamata disease].

Seishin Shinkeigaku Zasshi. 2007

[3]
Methylmercury-induced neural degeneration in rat dorsal root ganglion is associated with the accumulation of microglia/macrophages and the proliferation of Schwann cells.

J Toxicol Sci. 2019

[4]
Minamata disease revisited: an update on the acute and chronic manifestations of methyl mercury poisoning.

J Neurol Sci. 2007-11-15

[5]
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Environ Int. 2014-3-31

[6]
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Biochem Biophys Res Commun. 2018-6-2

[7]
Methylmercury exposure during the vulnerable window of the cerebrum in postnatal developing rats.

Environ Res. 2020-6-9

[8]
Involvement of enhanced sensitivity of N-methyl-D-aspartate receptors in vulnerability of developing cortical neurons to methylmercury neurotoxicity.

Brain Res. 2001-5-18

[9]
Does methylmercury-induced hypercholesterolemia play a causal role in its neurotoxicity and cardiovascular disease?

Toxicol Sci. 2012-8-17

[10]
Biomarkers of exposure and effect as indicators of the interference of selenomethionine on methylmercury toxicity.

Toxicol Lett. 2007-3-8

引用本文的文献

[1]
Methylmercury exposure at dosage conditions that do not affect growth can impair memory in adolescent mice.

Toxicol Res. 2024-4-27

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