Vitamin C and vitamin E supplementation reduce oxidative stress-induced embryo toxicity and improve the blastocyst development rate

Fertil Steril. 2002 Dec;78(6):1272-7. doi: 10.1016/s0015-0282(02)04236-x.

Abstract

To evaluate the adverse effects of exogenously induced reactive oxygen species (ROS) on mouse embryo development by using the 12-phorbol 13-myristate acetate (PMA)-activated leukocyte model as a source of ROS, and to examine the protective effect of antioxidant supplementation (vitamin C and vitamin E). Prospective study. Research laboratory. Effects of ROS on the blastocyst development rate in the presence and absence of antioxidant supplementation. After incubation with the PMA-activated leukocyte supernatant, the median (25th, 75th percentile) rate of blastocyst development significantly decreased from 73% (60%, 80%) after 3 hours to 30% (20%, 40%) after 6 hours compared with control reactions (86% [80%, 100%]). Co-incubating the embryos with vitamin C (50 microM) and the PMA-activated supernatant significantly increased the blastocyst development rate from 73% (60%, 80%) to 90% (80%, 91%) at 3 hours and from 30% (20%, 40%) to 91% (89%, 91%) at 6 hours-a level similar to that of control reactions. The blastocyst development rate increased after vitamin E supplementation (400 microM) at 6 hours, but not significantly and not by as much as after vitamin C supplementation. Exposure of mouse embryos to ROS for extended periods results in embryotoxicity. Vitamin C is more effective than vitamin E in reversing ROS-induced mouse embryo toxicity.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Antioxidants / pharmacology*
  • Ascorbic Acid / pharmacology*
  • Culture Techniques
  • Embryo, Mammalian / drug effects
  • Embryonic and Fetal Development / drug effects*
  • Embryonic and Fetal Development / physiology*
  • Female
  • Humans
  • Mice
  • Oxidative Stress / drug effects*
  • Oxidative Stress / physiology*
  • Prospective Studies
  • Reactive Oxygen Species / antagonists & inhibitors
  • Reactive Oxygen Species / pharmacology
  • Tetradecanoylphorbol Acetate / pharmacology
  • Vitamin E / pharmacology*

Substances

  • Antioxidants
  • Reactive Oxygen Species
  • Vitamin E
  • Tetradecanoylphorbol Acetate
  • Ascorbic Acid