首页> 外文期刊>The Journal of Reproduction and Development >Spermatogenic defects in a new inbred strain SD/gShi male rat with small testes.
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Spermatogenic defects in a new inbred strain SD/gShi male rat with small testes.

机译:新近交系SD / gShi雄性大鼠小睾丸的生精缺陷。

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A new inbred strain SD/gShi male rat with small testes was studied from the reproductive, histopathological and endocrinological viewpoints from 3 to 35 weeks of age. SD/gShi males showed only a slight increase in sperm production at puberty, in contrast to a rapid increase in normal SD males. At 6 weeks of age, spermiation became detectable in both SD/gShi and normal SD males, however, the numbers of spermatocytes and round spermatids per Sertoli cell in SD/gShi males were less than those in normal SD males. Moreover, the number of round spermatids per Sertoli cell did not increase in SD/gShi males at puberty, while they did in normal SD males. Histological analysis of germ cell numbers in SD/gShi males indicated that the lower numbers of spermatocytes and spermatids are caused by suppression of germ cell proliferation at the step from the spermatogonium to the preleptotene spermatocyte. Adult SD/gShi males showed normal fertilization ability, however, they had only 10-20% of sperm production innormal adult SD males and showed depressed sperm motion. Plasma total testosterone in SD/gShi males was lower for all ages, though testis testosterone concentration was normal. Plasma gonadotropin concentrations, especially FSH, remained higher than innormal SD males, indicating that the spermatogenic defects were not caused by gonadotropin deficiency. It is concluded that the SD/gShi male is characterized by spermatogenic defects at the preleptotene spermatocyte step which occur from the first spermatogenic wave. The SD/gShi male rat can serve as a useful model for studying spermatogenesis in rats.
机译:从生殖,组织病理学和内分泌学的角度研究了3至35周龄的新近交系SD / gShi雄性大鼠小睾丸。 SD / gShi男性在青春期精子产量仅略有增加,而正常SD男性则迅速增加。在6周龄时,SD / gShi男性和正常SD男性都可以检测到精子化,但是,SD / gShi男性中每个支持细胞的精母细胞和圆形精子数量少于正常SD男性。此外,在青春期SD / gShi雄性中,每个支持细胞的圆形精子数量没有增加,而在正常SD雄性中则增加。 SD / gShi雄性生殖细胞数量的组织学分析表明,精子细胞和精子细胞数量减少是由于从精原细胞到前瘦素精子细胞步骤的生殖细胞增殖受到抑制所致。成年SD / gShi男性表现出正常的受精能力,但是,他们只有正常成年SD男性精子产生的10-20%,并且表现出精子运动受阻。尽管睾丸睾丸激素浓度正常,SD / gShi男性的血浆总睾丸激素水平较低。血浆促性腺激素浓度,尤其是FSH仍高于正常SD男性,表明生精缺陷并非由促性腺激素缺乏引起。可以得出结论,SD / gShi男性的特征是在前瘦素的精子细胞步骤的精子形成缺陷,该缺陷是由第一次生精波产生的。 SD / gShi雄性大鼠可以作为研究大鼠精子发生的有用模型。

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