Burggren Warren W, Elmonoufy Nourhan A
Department of Biological Sciences, University of North Texas, Denton, TX, United States of America.
PLoS One. 2017 Sep 19;12(9):e0183649. doi: 10.1371/journal.pone.0183649. eCollection 2017.
Hypoxia during embryonic growth in embryos is frequently a powerful determinant of development, but at least in avian embryos the effects appear to show considerable intra- and inter-specific variation. We hypothesized that some of this variation may arise from different protocols that may or may not result in exposure during the embryo's critical window for hypoxic effects. To test this hypothesis, quail embryos (Coturnix coturnix) in the intact egg were exposed to hypoxia (~15% O2) during "early" (Day 0 through Day 5, abbreviated as D0-D5), "middle" (D6-D10) or "late" (D11-D15) incubation or for their entire 16-18 day incubation ("continuous hypoxia") to determine critical windows for viability and growth. Viability, body mass, beak and toe length, heart mass, and hematology (hematocrit and hemoglobin concentration) were measured on D5, D10, D15 and at hatching typically between D16 and D18 Viability rate was ~50-70% immediately following the exposure period in the early, middle and late hypoxic groups, but viability improved in the early and late groups once normoxia was restored. Middle hypoxia groups showed continuing low viability, suggesting a critical period from D6-D10 for embryo viability. The continuous hypoxia group experienced viability reaching <10% after D15. Hypoxia, especially during late and continuous hypoxia, also inhibited growth of body, beak and toe when measured at D15. Full recovery to normal body mass upon hatching occurred in all other groups except for continuous hypoxia. Contrary to previous avian studies, heart mass, hematocrit and hemoglobin concentration were not altered by any hypoxic incubation pattern. Although hypoxia can inhibit embryo viability and organ growth during most incubation periods, the greatest effects result from continuous or middle incubation hypoxic exposure. Hypoxic inhibition of growth can subsequently be "repaired" by catch-up growth if a final period of normoxic development is available. Collectively, these data indicate a critical developmental window for hypoxia susceptibility during the mid-embryonic period of development.
胚胎发育过程中的缺氧常常是发育的一个重要决定因素，但至少在鸟类胚胎中，其影响似乎表现出相当大的种内和种间差异。我们推测，这种差异的一部分可能源于不同的实验方案，这些方案可能导致也可能不会导致胚胎在对缺氧影响的关键窗口期受到暴露。为了验证这一假设，将完整鸡蛋中的鹌鹑胚胎（日本鹌鹑）在“早期”（第0天至第5天，简称为D0 - D5）、“中期”（D6 - D10）或“晚期”（D11 - D15）孵化期间或在整个16 - 18天的孵化期内（“持续缺氧”）暴露于缺氧环境（约15%氧气）中，以确定生存能力和生长的关键窗口期。在D5、D10、D15以及通常在D16至D18孵化时测量生存能力、体重、喙和趾长、心脏重量以及血液学指标（血细胞比容和血红蛋白浓度）。在早期、中期和晚期缺氧组的暴露期结束后，生存概率立即约为50 - 70%，但在早期和晚期组恢复常氧后生存能力有所提高。中期缺氧组的生存能力持续较低，表明D6 - D10是胚胎生存能力的关键时期。持续缺氧组在D15后生存概率降至<10%。在D15测量时，缺氧，尤其是晚期和持续缺氧，也会抑制身体、喙和趾的生长。除了持续缺氧组外，所有其他组在孵化时体重都能完全恢复到正常水平。与之前的鸟类研究相反，任何缺氧孵化模式都不会改变心脏重量、血细胞比容和血红蛋白浓度。尽管缺氧在大多数孵化期会抑制胚胎生存能力和器官生长，但最大的影响来自持续或中期孵化期的缺氧暴露。如果有一段常氧发育的末期，缺氧对生长的抑制随后可以通过追赶生长来“修复”。总体而言，这些数据表明在胚胎发育中期存在一个对缺氧敏感性的关键发育窗口。
