[Influence of peritoneal fluid with endometriosis on the development of mouse embryos]

To clarify the mechanism of infertility associated with endometriosis (EM), the effect of peritoneal fluid (PF) on early embryogenesis was examined. The addition of PF (5%) had no effect on the development of mouse 2-cell embryos. Since the PF is supposed to enter the oviductal cavity, PF may influence reproductive processes by modulating the intraoviductal microenvironment. As expected, PF with EM inhibited the development of 2-cell embryos co-cultured with oviducts whereas PF without EM had no effect. An increase in interleukin 1 (IL-1) has been identified in PF with EM. As with PF with EM, IL-1 inhibited the development of 2-cell embryos inasmuch as the oviducts were co-cultured. Indomethacin, an inhibitor of prostaglandin (PG) synthesis, effectively abolished the inhibitory action of both PF with EM and IL-1 on embryonic development. Moreover, PGE2 directly inhibited embryonic development. PGE2 was shown to inhibit the synthesis of protein by early embryos. These results demonstrate that PF with EM inhibits the development of early mouse embryos by acting on the oviducts. From these results it seems that an increase in IL-1 may be a causative factor in the embryo-toxic properties of PF with EM. We further suggest that PGE2 secreted from the oviducts by stimulation with PF with EM, may be an ultimate contributing factor in embryo-toxicity by inhibiting protein synthesis by early embryos.