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低水平亚慢性甲基汞暴露可降低大鼠的丁酰胆碱酯酶活性。

Sub-chronic exposure to methylmercury at low levels decreases butyrylcholinesterase activity in rats.

机构信息

Department of Clinical, Toxicological and Bromatological Analysis, Faculty of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.

出版信息

Basic Clin Pharmacol Toxicol. 2010 Feb;106(2):95-9. doi: 10.1111/j.1742-7843.2009.00475.x. Epub 2009 Oct 27.

DOI:10.1111/j.1742-7843.2009.00475.x
PMID:19874286
Abstract

In this study, we examined the effects of low levels and sub-chronic exposure to methylmercury (MeHg) on butyrylcholinesterase (BuChE) activity in rats. Moreover, we examined the relationship between BuChE activity and oxidative stress biomarkers [delta-aminolevulinic acid dehydratase (delta-ALA-D) and malondialdehyde levels (MDA)] in the same animals. Rats were separated into three groups (eight animals per group): (Group I) received water by gavage; (Group II) received MeHg (30 microg/kg/day) by gavage; (Group III) received MeHg (100 microg/kg/day). The time of exposure was 90 days. BuChE and ALA-D activities were measured in serum and blood, respectively; whereas MDA levels were measured in plasma. We found BuChE and ALA-D activities decreased in groups II and III compared to the control group. Moreover, we found an interesting negative correlation between plasmatic BuChE activity and MDA (r = -0.85; p < 0.01) and a positive correlation between plasmatic BuChE activity and ALA-D activities (r = 0.78; p < 0.01), thus suggesting a possible relationship between oxidative damage promoted by MeHg exposure and the decrease of BuChE activity. In conclusion, long-term exposure to low doses of MeHg decreases plasmatic BuChE activity. Moreover, the decrease in the enzyme is strongly correlated with the oxidative stress promoted by the metal exposure. This preliminary finding highlights a possible mechanism for MeHg to reduce BuChE activity in plasma. Additionally, this enzyme could be an auxiliary biomarker on the evaluation of MeHg exposure.

摘要

在这项研究中,我们研究了低水平和亚慢性甲基汞(MeHg)暴露对大鼠丁酰胆碱酯酶(BuChE)活性的影响。此外,我们还研究了同一批动物的 BuChE 活性与氧化应激生物标志物[δ-氨基-γ-酮戊酸脱水酶(δ-ALA-D)和丙二醛水平(MDA)]之间的关系。大鼠被分为三组(每组 8 只):(I 组)通过灌胃给予水;(II 组)通过灌胃给予 MeHg(30μg/kg/天);(III 组)通过灌胃给予 MeHg(100μg/kg/天)。暴露时间为 90 天。BuChE 和 ALA-D 活性分别在血清和血液中测量;而 MDA 水平在血浆中测量。我们发现与对照组相比,II 组和 III 组的 BuChE 和 ALA-D 活性降低。此外,我们发现血浆 BuChE 活性与 MDA 之间存在有趣的负相关(r = -0.85;p <0.01),与 ALA-D 活性之间存在正相关(r = 0.78;p <0.01),这表明 MeHg 暴露引起的氧化损伤与 BuChE 活性降低之间可能存在关系。总之,长期低剂量暴露于 MeHg 会降低血浆 BuChE 活性。此外,酶的减少与金属暴露引起的氧化应激强烈相关。这一初步发现强调了 MeHg 降低血浆 BuChE 活性的可能机制。此外,这种酶可能是评估 MeHg 暴露的辅助生物标志物。

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