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Most sterility outcomes may be associated with the presence of an inflammatory response due to infections. This environment would lead to an inability of the endometrium to implant, protect and maintain viable embryos. We have established an animal model of inflammation in which the systemic administration of bacterial endotoxin (LPS) results in a low embryo implantation rate.

OBJECTIVES:  To investigate the effect of the inflammatory agent LPS on the embryo viability. To verify the ability of vitamin E (VE) in preventing the effect of LPS.

For preimplantation studies we used pregnant mice B6CBAF1 which were intraperitoneally (i.p.) inoculated with LPS alone or with liposomes containing different concentrations of VE 24 hr after LPS injection. The embryos were obtained from the oviduct and the preimplantation rate was evaluated.

The treatment of pregnant female mice with LPS inoculated i.p. produces a decrease in the number of preimplantational embryos in a concentration dependent manner: as compared with non-treated LPS mice (100%), we obtained a 50–35% of preimplantational embryos with LPS treated mice. This LPS effect can be partially reverted by the administration of VE in animals treated with 4 or 6 mg/kg of LPS, but not in 10 mg/kg LPS treated mice. Preliminary results show that inflammatory cytokines are secreted by i.p. macrophages in LPS treated mice. In the present work we demonstrate the ability of VE to avoid an inflammatory environment and to allow viability.