Assessing the effects of low boron diets on embryonic and fetal development in rodents using in vitro and in vivo model systems

To date, boron (B) essentiality has not been conclusively shown in mammals. This article summarizes the results of a series of in vitro and in vivo ex periments designed to investigate the role of B in mammalian reproduction. In the first study, rat darns were fed either a low (0.04 mu g B/g) or an a dequate (2.00 mu g B/g) B diet for 6 wk before breeding and through pregnan cy; reproductive outcome was monitored on gestation day 20. Although low di etary B significantly lowered maternal blood, liver, and bone B concentrati ons, it had no marked effects on fetal growth or development. The goal of t he second study was to assess the effects of B on the in vitro development of rat postimplantation embryos. Day 10 embryos collected from dams fed eit her the low or adequate B diets for at least 12 wk were cultured in serum c ollected from male rats exposed to one of the two dietary B treatments. Dam s fed the low B diet had a significantly reduced number of implantation sit es compared to darns fed the B-adequate diet. However, embryonic growth in vitro was not affected by B treatment. The aim of study 3 was to define the limits of boric acid (BA) toxicity on mouse preimplantation development in vitro. Two-cell mouse embryos were cultured in media containing graded lev els of BA (from 6 to 10,000 mu M). Impaired embryonic differentiation and p roliferation were observed only when embryos were exposed to high levels of BA (>2000 mu M), reflecting a very low level of toxicity of BA on early mo use embryonic development. Study 4 tested the effects of low (0.04 mu g B/g ) and adequate (2.00 mu g B/g) dietary B on the in vitro development of mou se preimplantation embryos. Two-cell embryos obtained from the dams were cu ltured in vitro for 72 h. Maternal exposure to the low B diet for 10, 12, a nd 16 wk was associated with a reduction in blastocyst formation, a reducti on in blastocyst cell number, and an increased number of degenerates. Colle ctively, these studies support the concept that B deficiency impairs early embryonic development in rodents.