Department of Cellular and Physiological Sciences, Faculty of Medicine, Life Sciences Institute, University of British Columbia, Vancouver, BC, Canada.
Alcohol Clin Exp Res. 2013 Jul;37(7):1074-81. doi: 10.1111/acer.12079. Epub 2013 Mar 12.
During late prenatal and early postnatal life, the reproductive system in males undergoes an extensive series of physiological and morphological changes. Prenatal ethanol (EtOH) 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 EtOH 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 EtOH-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 with 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 with 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 with PF and C males on PN18 and 20, and PAE males had fewer primary spermatocytes per tubule on PN18 and round spermatids per tubule on PN25 compared with 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 with PF and/or C males in young adulthood (PN55).
Maternal EtOH consumption appears to delay both reproductive development and the onset of spermatogenesis in male offspring, with effects persisting at least until young adulthood.
在胎儿晚期和新生儿早期，男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（EtOH）暴露对生殖系统的发育有明显影响，并对成年后的功能产生长期影响。本研究检验了以下假设，即产前 EtOH 暴露会延迟精子发生的开始。
利用胎儿酒精谱系障碍（FASD）的大鼠模型检查生精小管的发育和精子发生的开始。从自由喂养的对照组（C）、配对喂养组（PF）和产前乙醇喂养组（PAE）的母鼠中获得雄性后代，并在出生后（PN）第 5、15、18、20、25、35、45 和 55 天处死，以通过从新生儿早期到成年早期的睾丸形态计量分析研究形态变化。
与 PF 和/或 C 雄性相比，PAE 雄性从 PN15 到青春期（PN45）的相对（按体重调整）睾丸重量较低。此外，在 PN5 时，基底膜上的生精细胞（原始生殖细胞）较少，而在 PAE 中更多的生精细胞位于基底膜上并正在分裂，这表明细胞分裂和迁移过程延迟。同样，在 PN18 和 20 时，PAE 雄性的管腔开放的小管比例低于 PF 和 C 雄性，在 PN18 时，PAE 雄性的每个小管中的初级精母细胞较少，在 PN25 时，PAE 雄性的每个小管中的圆形精子细胞较少。最后，在成年早期（PN55），处于 VII 和 VIII 期的小管比例较低，此时成熟的精子细胞移至上皮的顶端并被释放。
母体 EtOH 消耗似乎会延迟雄性后代的生殖发育和精子发生的开始，并且至少在成年早期仍存在影响。
