[Effects of indomethacin, prostaglandin E2 and prostaglandin F2 alpha on hatching of mouse blastocysts].

Although synthesis and metabolism of prostaglandins (PGs) in various mammalian blastocysts have been investigated, their variations and mechanism of actions are still unknown. The present study, therefore, has been performed to investigate how PGs would participate in the hatching process. We added indomethacin, and antagonist to PG biosynthesis, to a culture medium and examined its effect on the hatching of mouse blastocysts in vitro. Furthermore, we studied the cases in which prostaglandin E2 (PGE2) or prostaglandin F2 alpha (PGF2 alpha) were added to the culture media. The results are as follows. The hatching was significantly inhibited by indomethacin at a concentration of 10(-4) M yet the inhibition was reversible. In the groups with 10(-4) M indomethacin and PGE2, no improvement was seen in the inhibition of hatching and, on the other hand, inhibition became dose-relatively more distinct. The inhibition was irreversible, indicating possible cytotoxic effect on blastocysts. In the groups with 10(-4) M indomethacin and PGF2 alpha, inhibition of the hatching was significantly improved when PGF2 alpha was added at a concentration of 10(-6) M or 10(-5) M in comparison with the group with 10(-4) M indomethacin. No significant difference was observed when 10(-4) M PGF2 alpha was added. The above results indirectly confirmed that mouse blastocysts, in the pre-implantation stage, metabolize arachidonic acid and possess PG producing ability. Furthermore, they indicated that PGs influence hatching and, in particular, PGF2 alpha possibly had an accelerating effect. It was also supposed that a high concentration of PGE2 would exert a cytotoxic effect on blastocysts.