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经口摄入甲基汞会改变成年大鼠的前列腺微环境。

Oral exposure to methylmercury modifies the prostatic microenvironment in adult rats.

机构信息

Department of Morphology, Institute of Biosciences, Univ Estadual Paulista, Botucatu, SP, Brazil.

出版信息

Int J Exp Pathol. 2012 Oct;93(5):354-60. doi: 10.1111/j.1365-2613.2012.00825.x.

DOI:10.1111/j.1365-2613.2012.00825.x
PMID:22974216
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3444991/
Abstract

Methylmercury (MeHg) is an environmental pollutant that is highly toxic to the central nervous system. As its effects on male reproductive system are poorly understood, this study was carried out to analyse the effects of MeHg on the rat prostate. To evaluate the MeHg toxicity on ventral prostate, three groups of adult male Wistar rats received oral doses of 0.5, 1.0 and 3.0 mg/kg MeHg, respectively, on a daily basis for 14 days. A fourth group was used as a control. The prostate weight was decreased in rats treated orally with 0.5 mg/kg MeHg compared to controls. Also, Hg concentration increased significantly in the prostate after treatments. There were reductions in serum testosterone levels and androgen receptor immunoreactivity in animals receiving 3.0 mg MeHg/kg. The stereological data showed changes in the prostatic epithelial, stromal and luminal compartments which varied according to the different doses. Histopathological alterations, such as chronic inflammation, stratified epithelial hyperplasia and epithelial inflammatory reactive atypia, were observed in the 0.5 mg/kg MeHg-treated group. Epithelial atrophy was observed in the 3.0 mg/kg MeHg-treated group. In conclusion, the MeHg affects prostatic homoeostasis resulting in histopathological changes that may be relevant in the pathogenesis of prostatic disease.

摘要

甲基汞(MeHg)是一种对中枢神经系统具有高度毒性的环境污染物。由于其对男性生殖系统的影响尚未得到充分了解,因此进行了这项研究,以分析 MeHg 对大鼠前列腺的影响。为了评估 MeHg 对前列腺腹侧叶的毒性,三组成年雄性 Wistar 大鼠分别接受 0.5、1.0 和 3.0mg/kg MeHg 的口服剂量,每天一次,持续 14 天。第四组作为对照组。与对照组相比,经口给予 0.5mg/kg MeHg 的大鼠前列腺重量降低。此外,治疗后前列腺中的汞浓度显著增加。接受 3.0mgMeHg/kg 的动物的血清睾酮水平和雄激素受体免疫反应性降低。体视学数据显示,前列腺上皮、基质和管腔室的变化因剂量不同而有所不同。在 0.5mg/kg MeHg 处理组中观察到慢性炎症、分层上皮增生和上皮炎症反应性异型性等组织病理学改变。在 3.0mg/kg MeHg 处理组中观察到上皮萎缩。总之,MeHg 影响前列腺的稳态,导致组织病理学变化,这些变化可能与前列腺疾病的发病机制有关。

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本文引用的文献

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Mercury and selenium interaction in vivo: effects on thioredoxin reductase and glutathione peroxidase.汞和硒在体内的相互作用:对硫氧还蛋白还原酶和谷胱甘肽过氧化物酶的影响。
Free Radic Biol Med. 2012 Feb 15;52(4):781-93. doi: 10.1016/j.freeradbiomed.2011.12.002. Epub 2011 Dec 13.
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Effects of methylmercury on male reproductive functions in Wistar rats.甲基汞对 Wistar 大鼠雄性生殖功能的影响。
Reprod Toxicol. 2011 May;31(4):431-9. doi: 10.1016/j.reprotox.2011.01.002. Epub 2011 Jan 22.
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Developmental immunotoxicity of methylmercury: the relative sensitivity of developmental and immune parameters.甲基汞的发育免疫毒性:发育和免疫参数的相对敏感性。
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Methylmercury induced toxicogenomic response in C57 and SWV mouse embryos undergoing neural tube closure.甲基汞在 C57 和 SWV 小鼠胚胎神经管闭合过程中引起的毒基因组反应。
Reprod Toxicol. 2010 Sep;30(2):284-91. doi: 10.1016/j.reprotox.2010.05.009. Epub 2010 May 20.
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Long-term effects of developmental exposure to di-n-butyl-phthalate (DBP) on rat prostate: proliferative and inflammatory disorders and a possible role of androgens.发育期暴露于邻苯二甲酸二丁酯(DBP)对大鼠前列腺的长期影响:增殖和炎症紊乱以及雄激素的可能作用
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Determination of trace elements in biological samples by inductively coupled plasma mass spectrometry with tetramethylammonium hydroxide solubilization at room temperature.室温下用氢氧化四甲铵增溶-电感耦合等离子体质谱法测定生物样品中的微量元素
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Methylmercury neurotoxicity is associated with inhibition of the antioxidant enzyme glutathione peroxidase.甲基汞的神经毒性与抗氧化酶谷胱甘肽过氧化物酶的抑制有关。
Free Radic Biol Med. 2009 Aug 15;47(4):449-57. doi: 10.1016/j.freeradbiomed.2009.05.013. Epub 2009 May 18.
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Mercury and human genotoxicity: critical considerations and possible molecular mechanisms.汞与人类遗传毒性:关键考量因素及可能的分子机制
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