Oral exposure to methylmercury modifies the prostatic microenvironment in adult rats

被引:19
作者
Fossato da Silva, Daniela A. [1 ]
Barbosa, Fernando, Jr. [2 ]
Scarano, Wellerson R.
机构
[1] Univ Estadual Paulista, UNESP, Dept Morphol, Inst Biosci, BR-18618000 Botucatu, SP, Brazil
[2] Univ Sao Paulo, Dept Clin, Fac Pharmaceut Sci Toxicol & Bromatol Anal, BR-14049 Ribeirao Preto, SP, Brazil
基金
巴西圣保罗研究基金会;
关键词
adult male rat; androgen receptor; index proliferation; methylmercury; reproductive toxicity; ventral prostate; VENTRAL PROSTATE; GLUTATHIONE-PEROXIDASE; MOLECULAR-MECHANISMS; METHYL MERCURY; CANCER; MICE; CARCINOGENESIS; NEUROTOXICITY; SPERMATOGENESIS; INFLAMMATION;
D O I
10.1111/j.1365-2613.2012.00825.x
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
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 3.0mg/kg MeHg, respectively, on a daily basis for 14days. A fourth group was used as a control. The prostate weight was decreased in rats treated orally with 0.5mg/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 3.0mgMeHg/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 0.5mg/kg MeHg-treated group. Epithelial atrophy was observed in the 3.0mg/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.
引用
收藏
页码:354 / 360
页数:7
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