• embryo viability;
  • inflammatory response;
  • lipopolysaccharyde;
  • oxidative stress

Problem:  Many sterility outcomes may be associated to the presence of an inflammatory response that would lead to an inability of the endometrium to support implantation and maintain viable embryos. We have established an animal model of inflammation in which the systemic administration of lipopolysaccharyde (LPS) results in a low embryo implantation rate. The purpose of this work was to investigate the effect of the inflammatory agent LPS on embryo viability and to verify the ability of vitamin E to modulate the inflammatory effect of LPS on embryo viability.

Method of study:  For pre-implantation studies B6CBAF1 mice, which were intraperitoneally inoculated with LPS (4–10 mg/kg), were used. Mice were also treated with vitamin E (4–10 mg/kg) before or after LPS injection. Embryos were obtained from the oviduct after each treatment.

Results:  The LPS produces a decrease in the number of pre-implantational embryos in a concentration dependent manner. The LPS effect can be partially reversed or prevented by vitamin E. Preliminary results show that inflammatory cytokines are secreted by intraperitoneal macrophages in LPS treated mice.

Conclusion:  Our results demonstrate the ability of vitamin E to avoid an inflammatory environment and to allow viability of embryos.