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亚硝酸盐暴露致雄性小鼠生殖毒性的探讨

发布时间:2018-03-29 01:15

  本文选题:亚硝酸盐 切入点:生殖毒性 出处:《解剖学报》2017年05期


【摘要】:目的探讨亚硝酸盐暴露对雄性小鼠生殖毒性的分子机制。方法 36只2月龄健康雄性小鼠,随机分为对照组(生理盐水)、低剂量组(60 mg/kg)和高剂量组(120 mg/kg),每组12只进行亚硝酸盐灌胃3个月,观察小鼠的生长状况,HE染色法观察睾丸组织病理变化,免疫荧光和Western blotting方法分析检测睾丸组织细胞增殖与凋亡情况及DNA甲基化、组蛋白去乙酰化相关酶的表达情况。结果亚硝酸盐暴露组小鼠较对照组小鼠体重增加缓慢,睾丸指数降低(P0.01),形态发生病理性改变;亚硝酸盐暴露组小鼠睾丸组织细胞增殖较对照组明显减少,细胞凋亡较对照组明显增加(P0.01);同时DNA甲基化和组蛋白去乙酰化水平高于对照组(P0.01),且均具有剂量依赖性。结论亚硝酸盐暴露通过抑制雄性小鼠生长发育及睾丸生精细胞增殖,诱导睾丸生精细胞凋亡,造成雄性生殖毒性;DNA甲基化及组蛋白去乙酰化水平升高,提示表观遗传学可能参与了亚硝酸盐暴露对雄性生殖系统的损伤过程及调控机制。
[Abstract]:Objective to explore the molecular mechanism of reproductive toxicity of nitrite exposure in male mice. They were randomly divided into two groups: control group (normal saline group), low dose group (60 mg / kg) and high dose group (120 mg / kg). 12 rats in each group were treated with nitrite for 3 months. The growth of mice was observed by HE staining method and the pathological changes of testicular tissue were observed. The proliferation and apoptosis of testicular cells and the expression of DNA methylation and histone deacetylation related enzymes were detected by immunofluorescence and Western blotting. Results the weight gain of nitrite exposed mice was slower than that of control mice. The testicular index decreased P0.01G and morphogenetic pathological changes, the proliferation of testicular cells in the nitrite exposed group was significantly lower than that in the control group. The levels of DNA methylation and histone deacetylation were higher than those of the control group in a dose-dependent manner. Conclusion nitrite exposure can inhibit the growth and development of male mice and the proliferation of spermatogenic cells. The apoptosis of testicular spermatogenic cells was induced and the DNA methylation and histone deacetylation level of male reproductive toxicity were increased, which suggested that epigenetics might be involved in the damage process and regulation mechanism of male reproductive system induced by nitrite exposure.
【作者单位】: 郑州大学基础医学院人体解剖学系;河南大学神经生物学研究所;
【基金】:高等学校博士学科点专项科研基金(20134101110014)
【分类号】:R698.2


本文编号:1678902

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