1α(OH)ase-/-小鼠睾丸组织内氧化应激增强导致精子发生障碍
孙伟伟，戴秀亮
基金项目：教育部博士学科点基金(KY1010231121211046) 作者简介：孙伟伟（1982），女，讲师，生殖医学.

（南京医科大学人体解剖学系，江苏南京 210000）
摘要：目的 探讨1,25(OH)2D3缺乏导致精子发生障碍的机制。方法 应用双向凝胶电泳（2-DE）和激光时间飞行质谱分析（MALDI-TOF/TOF）技术，结合生物信息分析，对正常饮食和纠正饮食后野生型（1α(OH)ase+/+）和纯合子小鼠（1α(OH)ase-/-）睾丸组织中的差异表达蛋白进行筛选，并选择其中一些关键蛋白质的进行功能分析。结论1,25(OH)2D3 缺乏通过介导细胞外钙、磷水平，影响1α(OH)ase-/- 小鼠睾丸组织内氧化应激水平，p53信号通路被激活，最终导致精子发生异常。
关键词：1,25(OH)2D3；精子发生；氧化应激；p53信号通路
中图分类号：R3

Enhanced oxidative stress found in testis from 1α(OH)ase-/- mice cause deficient spermatogenesis
SUN Weiwei, DAI Xiuliang
(Anatomy Departemnt of Nanjing Medical University, Jiangsu Nanjing 210000)
Abstract: To further investigate possible mechanism whereby 1,25(OH)2D3 deficiency increased  the apoptosis of spermatogenic cells, alterations of testis protein expression between 1α(OH)ase+/+ and 1α(OH)ase-/- mice fed with either normal diet or rescue diet were examined by 2-Dimentional electrophoresis and mass chromatographic analysis, functional analysis of some key protein were performed. The results indicated that the absence of 1,25(OH)2D3 mediated by exracellular calciun and phosphorus influenced oxidative stress of mutant testis, induced p53  signal pathway, resulted in deficient spermatogenesis.
Key words: 1,25(OH)2D3；spermatogenesis; oxidative stress; p53 signal pathway