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早期甲状腺功能减退恢复过程中大鼠睾丸生精小管生长和精子发生的增强:一项定量研究。

Enhancement of seminiferous tubular growth and spermatogenesis in testes of rats recovering from early hypothyroidism: a quantitative study.

作者信息

Meisami E, Najafi A, Timiras P S

机构信息

Division of Developmental and Cell Biology, University of California, Berkeley 94720.

出版信息

Cell Tissue Res. 1994 Mar;275(3):503-11. doi: 10.1007/BF00318819.

Abstract

Testicular weight and DNA content were markedly reduced (63 and 69%) in weanling Long-Evans rat pups rendered hypothyroid from birth by administration of propylthiouracil (PTU), a reversible goitrogen. These growth deficits worsened to > 80% by continuing hypothyroidism beyond weaning, to days 50 and 90. Recovery of thyroid function, brought about by discontinuing PTU at weaning, resulted in a paradoxical stimulation of testis growth, amounting to increased weight (40%), DNA content (60%) and size by 90 days, compared to age-matched controls. In the 25-day or older hypothyroid rats, testicular structure was immature and spermatogenesis markedly delayed, as evident by closed lumen and significantly reduced diameter of seminiferous tubules (38%), thickness of germinal layer (70%), and number of primary spermatocytes (86%), compared to control. Hypothyroidism did not alter the number of tubules per testis cross section. In the 90-day recovery rats, numbers of seminiferous tubules were unchanged but tubular diameter was significantly (20%) larger than in controls and spermatogenesis appeared very active as indicated by significantly increased germinal layer thickness (22%) and total number and density of primary spermatocytes (55% and 40%). The results show that although postnatal hypothyroidism is deleterious for testicular growth and spermatogenesis, recovery from this condition leads to enhanced seminiferous tubular growth and spermatogenesis.

摘要

通过给予丙硫氧嘧啶(PTU,一种可逆性致甲状腺肿物质)使新生的Long-Evans断奶大鼠幼崽从出生起就甲状腺功能减退,其睾丸重量和DNA含量显著降低(分别为63%和69%)。如果断奶后持续甲状腺功能减退至50天和90天,这些生长缺陷会恶化至超过80%。断奶时停止给予PTU使甲状腺功能恢复,结果却反常地刺激了睾丸生长,到90天时,与年龄匹配的对照组相比,睾丸重量增加了40%,DNA含量增加了60%,大小也有所增加。在25日龄及以上的甲状腺功能减退大鼠中,睾丸结构不成熟,精子发生明显延迟,与对照组相比,可见管腔闭合、生精小管直径显著减小(38%)、生发层厚度显著减小(70%)以及初级精母细胞数量显著减少(86%)。甲状腺功能减退并未改变每个睾丸横截面上的小管数量。在90日龄的恢复组大鼠中,生精小管数量未变,但管腔直径比对照组显著增大(20%),并且精子发生看起来非常活跃,表现为生发层厚度显著增加(22%)以及初级精母细胞总数和密度显著增加(分别为55%和40%)。结果表明,虽然出生后甲状腺功能减退对睾丸生长和精子发生有害,但从这种状态恢复会导致生精小管生长和精子发生增强。

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