title: Prenatal ethanol exposure delays the onset of spermatogenesis in the rat.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Cellular and Physiological Sciences, Faculty of Medicine, Life Sciences Institute, University of British Columbia, Vancouver, BC, Canada. lanni.lan@gmail.com
authors.forename: Ni
authors.initials: N
authors.lastname: Lan
authors.forename: A Wayne
authors.initials: AW
authors.lastname: Vogl
authors.forename: Joanne
authors.initials: J
authors.lastname: Weinberg
mesh_terms: D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D000431:Ethanol / Q000008:administration & dosage / Q000633:toxicity*; D005260:Female; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000097:blood / Q000139:chemically induced* / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012741:Sexual Maturation / Q000187:drug effects* / Q000502:physiology; D013091:Spermatogenesis / Q000187:drug effects* / Q000502:physiology; D013739:Testosterone / Q000097:blood
chemical_list: D000431:Ethanol; D013739:Testosterone
keywords: Fetal Alcohol Spectrum Disorder; Prenatal Ethanol Exposure; Reproductive Development; Spermatogenesis