Mechanism of transcription of phospholipid glutathione peroxidase

非线粒体PHGPx在肾细胞、L929细胞等体细胞中高表达，而线粒体PHGPx在这些细胞中的表达水平较低。线粒体PHGPx在小鼠睾丸发育3周时开始表达。而线粒体PHGPx在肾脏中未被诱导表达。线粒体PHGPx启动子活性约为总PHGPx活性的三分之一。线粒体PHGPx核心启动子区域为-233 ~ -158区域，包含SP1位点。而非线粒体PHGPx的核心启动子位于NFY位点、CCAAT盒和AP2位点所在的-176 ~ -56区域。PHGPx在人精子中段的线粒体中强烈表达。我们发现一些不育雄性精子中PHGPx的表达水平显著下降。在我们调查的73名不育男性中，这些人约占10%。所有7例有phgpx缺陷精子的患者都被归类为少弱精子症，精子数量和活力都明显低于正常水平。有phgpx缺陷精子的男性占27例少弱精子症不育男性的35%。31例可育志愿者精子中未见PHGPx表达缺陷。电镜下线粒体超微结构分析显示，phgpx缺陷精子线粒体形态异常。提示精子中线粒体PHGPx表达缺失可能是不育男性少弱精子症的原因之一。

Non-mitochondrial PHGPx was highly expressed in somatic cells such as kidney cells and L929 cells, while the expression of mitochondrial PHGPx was quite low in these cells. Expression of mitochondrial PHGPx was initiated in the 3 weeks development-stage of testis of mice. However, expression of mitochondrial PHGPx was not induced in kidney. Activity of promoter of mitochondrial PHGPx was almost one third of that of total PHGPx. The region of core promoter of mitochondrial PHGPx was the region from -233 to -158 which included SP1 site. While core promoter of non-mitochondrial PHGPx was found in the region from -176 to -56 in which NFY site, CCAAT box and AP2 site.PHGPx was intensely expressed in mitochondria in the mid-piece of human spermatozoa. We found a dramatic decrease in the level of expression of PHGPx in the spermatozoa of some infertile males. These individuals accounted for about 10% of the group of 73 infertile males that we examined. All seven patients with PHGPx-defective spermatozoa were classified as suffering from oligo-asthenozoospermia, a defect in which both the number and the motility of spermatozoa are significantly below normal. Males with PHGPx-defective spermatozoa accounted for 35% of the 27 infertile males with oligo-asthenozoospermia. No defects in expression of PHGPx in spermatozoa were observed in 31 fertile volunteers. Ultrastructual analysis of mitochondria by electron microscopy demonstrated that the morphology of mitochondria in PHGPx-defective spermatozoa was abnormal. The results suggest that failure of the expression of mitochondrial PHGPx in spermatozoa might be one of the causes of oligo-asthenozoospermia in infertile men.