Prenatal ethanol exposure delays the onset of spermatogenesis in the rat.
Prenatal ethanol exposure delays the onset of spermatogenesis in the rat.
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DOI：
10.1111/acer.12079
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发表时间：
2013-07
期刊：
影响因子：
--
通讯作者：
Weinberg J
中科院分区：
文献类型：
--
作者：
Lan N;Vogl AW;Weinberg J
在出生前晚期和出生后早期，雄性生殖系统经历了一系列广泛的生理和形态变化。产前乙醇暴露对生殖系统的发育有显著影响，对成年期的功能有长期影响。本研究验证了产前酒精暴露会延迟精子发生的假设。利用胎儿酒精谱系障碍（FASD）大鼠模型研究生精小管的发育和精子发生的开始。在出生后（PN）第5、15、18、20、25、35、45和55天处死自由采食对照组（C）、成对饲喂组（PF）和乙醇饲喂（产前酒精暴露，PAE）母鼠的雄性后代，通过对新生儿早期至成年期的睾丸进行形态学分析，研究其形态学变化。从PN 15至青春期（PN 45），PAE雄性动物的相对（根据体重调整）睾丸重量低于PF和/或C雄性动物。此外，更少的生殖细胞（原始生殖细胞）位于基板上的PN 5，而更多的接触基板分裂的PAE相比，PF和C男性，这表明延迟细胞分裂和迁移过程。此外，在PN 18和PN 20时，PAE中管腔开放的小管百分比低于PF和C雄性，并且与C雄性相比，PAE雄性在PN 18时每个小管的初级精母细胞较少，在PN 25时每个小管的圆形精子细胞较少。最后，在阶段VII和VIII，当成熟的精子细胞移动到上皮细胞的顶端并被释放时，小管的百分比在PAE中低于PF和/或C男性在成年初期（PN 55）。母亲的乙醇消费似乎延迟生殖发育和男性后代精子发生的开始，其影响至少持续到成年早期。
During late prenatal and early postnatal life, the reproductive system in males undergoes an extensive series of physiological and morphological changes. Prenatal ethanol exposure has marked effects on the development of the reproductive system, with long-term effects on function in adulthood. The present study tested the hypothesis that prenatal ethanol exposure will delay the onset of spermatogenesis. Development of the seminiferous tubules and the onset of spermatogenesis were examined utilizing a rat model of fetal alcohol spectrum disorder (FASD). Male offspring from ad libitum-fed control (C), pair-fed (PF) and ethanol-fed (prenatal alcohol exposure, PAE) dams were terminated on postnatal (PN) days 5, 15, 18, 20, 25, 35, 45 and 55, to investigate morphological changes through morphometric analysis of the testes from early neonatal life through young adulthood. PAE males had lower relative (adjusted for body weight) testis weights compared to PF and/or C males from PN15 through puberty (PN45). In addition, fewer gonocytes (primordial germ cells) were located on the basal lamina on PN5, while more of those touching the basal lamina were dividing in PAE compared to PF and C males, suggesting delayed cell division and migration processes. As well, the percentage of tubules with open lumena was lower in PAE compared to PF and C males on PN18 and PN20, and PAE males had fewer primary spermatocyte per tubule on PN18 and round spermatids per tubule on PN25 compared to C males. Finally, the percentage of tubules at stages VII and VIII, when mature spermatids move to the apex of the epithelium and are released, was lower in PAE compared to PF and/or C males in young adulthood (PN55). Maternal ethanol consumption appears to delay both reproductive development and the onset of spermatogenesis in male offspring, with effects persisting at least until young adulthood.
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影响因子：
2.9
作者：
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