Melatonin ameliorates the fertilization capacity of oocytes exposed to 17α-ethynylestradiol

Reprod Toxicol. 2020 Apr:93:61-67. doi: 10.1016/j.reprotox.2020.01.004. Epub 2020 Jan 10.

Abstract

17α-ethynylestradiol (EE2), a synthetic hormone that derives from the natural hormone estradiol, has been reported to alter the sex determination, sexual maturity and secondary sexual characteristics of exposed organisms. However, the adverse effects of EE2 on the oocyte quality have not fully determined. Here, we found that EE2 exposure compromised the fertilization capacity of mouse oocytes, while treatment of melatonin remarkably elevated the fertilization rate. Specifically, we observed that EE2 exposure led to the abnormal distribution and premature exocytosis of ovastacin, leading to the reduced number of sperm binding to the EE2-exposed oocytes. In addition, we found that the abundance of Juno, the sperm receptor on the oocyte membrane, was also diminished, which might be another potential cause leading to the fertilization failure of EE2-exposed oocytes. Finally, we demonstrated that melatonin improved the fertilization ability of EE2-exposed oocytes through eliminating the excessive ROS and inhibiting apoptosis.

Keywords: Apoptosis; EE2; Fertilization capacity; Juno; Melatonin; Ovastacin; ROS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Ethinyl Estradiol / pharmacology*
  • Female
  • Fertilization / drug effects*
  • Male
  • Melatonin / pharmacology*
  • Mice, Inbred ICR
  • Oocytes / drug effects*
  • Oocytes / physiology
  • Reactive Oxygen Species / metabolism
  • Receptors, Cell Surface / metabolism
  • Spermatozoa / drug effects
  • Spermatozoa / physiology

Substances

  • Reactive Oxygen Species
  • Receptors, Cell Surface
  • folate receptor 4, mouse
  • Ethinyl Estradiol
  • Melatonin