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甲基汞暴露母体对子代大鼠脊髓神经退行性变及髓鞘碱性蛋白表达下调的影响

Methylmercury Causes Neurodegeneration and Downregulation of Myelin Basic Protein in the Spinal Cord of Offspring Rats after Maternal Exposure.

机构信息

Laboratory of Functional and Structural Biology, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, PA, Brazil.

Graduate Program in Health and Society, University of the State of Rio Grande do Norte, Mossoró 59610-210, RN, Brazil.

出版信息

Int J Mol Sci. 2022 Mar 29;23(7):3777. doi: 10.3390/ijms23073777.

Abstract

Methylmercury (MeHg) is one of the most dangerous toxic pollutants spread throughout the earth. Chronic MeHg intoxication by contaminated food ingestion is the most common threat to human health, including impairment to the developing fetus. The present study aims at investigating the effects of maternal exposure to MeHg during gestation and lactation on the spinal cord of offspring. Pregnant rats received oral doses of MeHg (40 μg/kg/day) over a period of 42 days (21 gestation and 21 lactation). Control animals received the vehicle only. Total mercury concentration was measured in blood samples from offspring collected at the 41st postnatal day. Counting of motor neurons and immunoreactivity for myelin basic protein (MBP) were assessed in the spinal cords in both control and MeHg-intoxicated animals. Our results showed that MeHg promoted an increase in blood Hg levels. In addition, it caused a reduction in the number of spinal cord motor neurons as well as decreased MBP immunoreactivity in the cervical, thoracic and lumbar segments. Our present findings suggest that MeHg intoxication during rat pregnancy and lactation is associated with a pattern of motor neuron degeneration and downregulation of myelin basic protein in different segments of a developing spinal cord. Further studies are needed to establish the effect of MeHg intoxication in both young and adult rats.

摘要

甲基汞(MeHg)是分布在全球范围内最危险的有毒污染物之一。通过受污染的食物摄入慢性甲基汞中毒是对人类健康最常见的威胁,包括对发育中的胎儿造成损害。本研究旨在探讨母体在妊娠和哺乳期暴露于甲基汞对后代脊髓的影响。怀孕大鼠在 42 天的时间内(21 天妊娠和 21 天哺乳期)接受口服甲基汞(40μg/kg/天)的剂量。对照组动物仅接受载体。在出生后第 41 天收集后代的血液样本,测量血液中的总汞浓度。在对照组和甲基汞中毒组动物的脊髓中评估运动神经元计数和髓鞘碱性蛋白(MBP)的免疫反应性。我们的研究结果表明,甲基汞促进了血液中汞水平的升高。此外,它还导致脊髓运动神经元数量减少,颈部、胸部和腰部脊髓节段的 MBP 免疫反应性降低。我们目前的研究结果表明,大鼠妊娠和哺乳期的甲基汞中毒与发育中脊髓不同节段的运动神经元退化和髓鞘碱性蛋白下调模式有关。需要进一步的研究来确定幼年和成年大鼠中甲基汞中毒的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17ff/8998727/e1d4460851f9/ijms-23-03777-g001.jpg

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