Studies say that the sexual function of male rodents can be impaired by in utero and/or neonatal exposure to external molecules that disrupt normal hormone functioning.
This would give rise to concerns that low-level exposure to such molecules might cause similar effects in humans.
Examples of such molecules include the synthetic nonsteroidal estrogen DES, which was used as a treatment for various diseases until the mid 1990s, and BPA, which is found, among other places, in some plastic containers. New research, by David H. Volle and colleagues, at INSERM U895, France, has identified the molecular mechanism underlying many of the harmful effects of DES on the mouse testis.
The pivotal experiments demonstrated that neonatal exposure to DES led to a much more dramatic reduction in fertility in male mice with the protein NR0B2 than it did in male mice lacking the protein because NR0B2 deficiency protected male mice against the negative effects of DES on testis development and function. NR0B2 deficiency also protected male mice from the detrimental effects of postnatal and adult exposure to DES. Future work will determine whether similar pathways link human exposure to molecules such as DES that disrupt normal hormone functioning to the increased incidence of male reproductive disorders.