双酚A对诱导型一氧化氮合酶基因缺失鼠卵母细胞染色体不分离的影响

目的:研究双酚A(bisphenol A,BPA)暴露对诱导型一氧化氮合酶(inducible nitric oxide synthase,i Nos)基因缺失(i Nos-/-)的实验鼠卵母细胞染色体不分离的影响。方法:给野生型雌鼠(i Nos+/+)和i Nos基因敲除(i Nos-/-)的雌鼠强饲(oral gavage)BPA 100μg/(kg·d)或200μg/(kg·d)连续13 d。结果:在i Nos+/+组实验鼠卵细胞MⅡ期非整倍体卵母细胞数量没有显著增加。在i Nos-/-组实验鼠卵母细胞染色体分离错误和染色单体提前分离增加。基因表达的特性表明polo样激酶1(PLK1)和...

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Published in国际生殖健康/计划生育杂志 Vol. 34; no. 3; pp. 184 - 188
Main Author 张金文 杜春海 张杰
Format Journal Article
LanguageChinese
Published 河北医科大学第二医院血管外科, 石家庄,050000%河北省景县人民医院血管外科%河北医科大学第四医院妇瘤科 2015
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ISSN1674-1889

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Summary:目的:研究双酚A(bisphenol A,BPA)暴露对诱导型一氧化氮合酶(inducible nitric oxide synthase,i Nos)基因缺失(i Nos-/-)的实验鼠卵母细胞染色体不分离的影响。方法:给野生型雌鼠(i Nos+/+)和i Nos基因敲除(i Nos-/-)的雌鼠强饲(oral gavage)BPA 100μg/(kg·d)或200μg/(kg·d)连续13 d。结果:在i Nos+/+组实验鼠卵细胞MⅡ期非整倍体卵母细胞数量没有显著增加。在i Nos-/-组实验鼠卵母细胞染色体分离错误和染色单体提前分离增加。基因表达的特性表明polo样激酶1(PLK1)和RAN GTPase蛋白(RAN)水平在i Nos-/-组实验鼠卵细胞的细胞周期和纺锤体的调控大幅下降。结论:i Nos可能通过维持蛋白PLK1和蛋白RAN在哺乳类动物卵细胞稳定地表达,直接或间接地保护染色体减数分裂中精确分离;低水平的BPA暴露可能引起具有i Nos-/-遗传背景卵细胞染色体畸变。
Bibliography:Objective: To explore the effects of bisphenol A (bisphenol A, BPA) on the oocyte chromosome non-disjunction in iNos4- mice. Methods:Female iNos mice and iNos-/- mice, aged 20-22 days, were treated with BPA (100 or 200 μg/kg body weight per day) by intragastric administration for 13 days. The isopyknic corn oil was used as control. Results:In the iNos^+/+ mice groups, the numbers of aneuploidy oocytes at metaphase M Ⅱ were not increased by BPA treatment. Interestingly, the numbers of those oocytes with the error- prone chromosome segregation and the precocious chromatid separation in the iNos 4- mice groups were significantly increased by BPA treatment. Meanwhile, the expressions of polo-like kinase-1 (PLK1) and RAN GTPase (RAN) in oocytes of the iNos4- mice were significantly down-regulated by BPA treatment. Conclusions: iNos has a direct or indirect protection against the faithful chromosome segregation during meiosis, possibly by maintaining stable expression of PLK1 and RAN in mammalian oocytes. BPA expos
ISSN:1674-1889