The relationship between fertility and mutation on genome caused by oxidative damage during spermatogenesis

本课题研究了精子发生过程中氧化损伤引起的基因组突变与生育力的关系。我们使用C57 BL/6野生型小鼠以及Msh 2缺陷型小鼠。我们观察了睾丸切片的老化情况，并进行了照射。辐射会增加生殖细胞基因组DNA的氧化损伤。睾丸用bouins溶液固定，切片至5μm。结果：Msh 2基因缺陷小鼠睾丸重量随年龄增长而下降，睾丸重量随年龄增长而下降。14周龄后，Msh 2基因缺陷小鼠睾丸重量为野生型的60%。切片观察显示生殖器退化，进入细线期前。生殖细胞在生殖期和细线期前出现明显的凋亡。我们推测睾丸重量的下降可能是由于生殖细胞的持续凋亡所致。尽管14周龄Msh 2缺陷小鼠后凋亡的生殖细胞数量增加，睾丸重量降低至野生型小鼠的60%，但它们显示正常的生育能力。

We have studied about the relationship between fertility and mutation on genome caused by oxidative damage during spermatogenesis. We used C57BL/6 wild type mice as well as Msh2 deficient mice. We have observed the testis section according to the aging and also we performed irradiation. Irradiation should increase the oxidative DNA damage on the genome of germ cells. Testis was fixed with bouins solution and sectioned to 5μm. We also observed fertility of Msh2 deficient mice.Results : The testis weight of Msh2 deficient mice was decreased according to the age. After 14 weeks old, the testis weight of Msh2 deficient mice become 60% of wild type one. The observation of section reveals degeneration of gonia and pre leptotene stage. Durin gonia and pre leptotene stage, we could observe significant apoptotic germ cells. We supposed the decrease of testis weight should be caused by the continuous apoptosis of germ cells. Although the apoptotic germ cell number increase after 14 weeks old Msh2 deficient mice and the weight of the testis decrease to 60% of wild type mice, they reveals normal fertility.