Adverse effects of a low boron environment on the preimplantation development of mouse embryos in vitro

We have used a preimplantation embryo culture system to investigate the eff ects of boron (B) deficiency on early mouse development. To test the influe nce of low boron concentration in the medium, two-cell embryos collected fr om CD-1 mice fed a commercial stock high boron diet were cultured for 72 h in control boron (B+), or boron-free (B-) media. Preimplantation developmen t was similar in the two groups over the 72-h period (Study 1). To investig ate the influence of maternal boron status on early embryonic development, mice were fed a low boron (0.04 mu g B/g, LOW), or a suppplemented boron (2 .05 mu g B/g, SUPP) purified diet, or a high boron (11.8 mu g B/g, STOCK) c ommercial stock diet. In Study 2A, two-cell embryos were collected after th e females had been fed the diets for 10, 12, or 16 weeks. Embryos were cult ured in B+ medium. In Study 2B, two-cell embryos were collected after the f emales had been fed the diets for 16 weeks, and the embryos were cultured i n B- medium. In both studies, liver and tibia boron concentrations were low er in LOW fed mice than in mice fed the SUPP or STOCK diets. The in vitro d evelopment of two-cell embryos collected from mice fed either one of the bo ron purified diets was not severely impaired when they were cultured in Bmedium. However, two-cell embryos from the LOW diet had a lower frequency o f blastocyst formation (83.5%, LOW vs. 90.1%, SUPP), and an increased frequ ency of degenerate embryos (13.0%, LOW vs. 8.0%, SUPP) after 72 h of cultur e compared to embryos from the SUPP diet. Exposure to dietary and medium bo ron deficiency significantly compromised the in vitro development of two-ce ll embryos compared to dietary boron deficiency alone. Low dietary boron co mbined with low boron in the medium resulted in the highest percentage of d egenerate embryos (57.0%). Collectively, these data support the concept tha t boron deficiency impairs early embryonic development in rodents. J. Trace Elem. Exp. Med. 12:235-250, 1999. (C) 1999 Wiley-Liss, Inc.