Current Zoology (Feb 2009)

Developmental competence and ultrastructural changes of heat-stressed mouse early blastocysts produced in vitro

  • Mingzhi WANG,
  • Zhongjie TIAN,
  • Tao LI,
  • Shansong GAO,
  • Zhongling JIANG,
  • Wenru TIAN,
  • Pingping QU,
  • Pingping QU,
  • Wenru TIAN,
  • Zhongling JIANG,
  • Shansong GAO,
  • Tao LI,
  • Zhongjie TIAN,
  • Mingzhi WANG

Journal volume & issue
Vol. 55, no. 1
pp. 61 – 66

Abstract

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Mouse early blastocysts were exposed to temperatures of 39℃ and 41℃ for 2 h, respectively, to determine their developmental competence and ultrastructural changes. The results showed that heat stress at 41℃ for 2 h, significantly reduced the percentages of expanded and hatched blastocysts, but not at 39℃ for 2 h. The average cell numbers in expanded blastocysts, which developed from early blastocysts heat-stressed at temperatures of 39℃ and 41℃, were significantly reduced. The average cell numbers in hatched blastocysts subjected to heat stress were no different from those in the control group cultured at 37℃. The mitochondria of the early blastocysts heat-stressed at 39℃ for 2 h, were slightly swollen, but they had recovered after culturing at 37℃ for 2 h. However, the mitochondria in the blastocysts heat stressed at 41℃ for 2 h were severely swollen, and their number increased. The ribosomes shed from the rough endoplasmic reticulum, and the number of secondary lysosomes in the plasma increased. The integrity of desmosomes was disrupted. The space between the nuclear envelope and the perivitelline membrane enlarged. The fibre fraction and the particulate fraction of nucleoli were separated. The heterochromatin in nucleoli was also increased in its quantity. There were some lamellar-shape structures and heterogeneous dense materials exhibiting in the cytoplasm. The ultrastructural changes induced by heat shock at 41℃ for 2 h were not reversible. In conclusion, the damage of heat stress to mitochondria, lysosomes, ribosomes and cell nucleus, may be one of the most important factors that inhibit the normal development of mouse early blastocysts [Current Zoology 55(1): 61–66, 2009].

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