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Adult exposure to bisphenol A alters male sexual behavior

There are human reproduction concerns associated with extensive use of bisphenol A (BPA) containing plastic. In this context, it remains unclear whether and how exposure to BPA interferes with the developmental organization and adult activation of male sexual behavior by testosterone. Here we show for the first time, that the neural circuitry underlying male sexual behavior is vulnerable to chronic adult exposure to low dose of BPA and suggests that BPA could act in vivo as an anti-androgenic compound.

canette contenant du bisphénol A. © INRA
Updated on 11/07/2014
Published on 10/28/2014

Context and challenge:

There are human reproduction concerns associated with extensive use of bisphenol A (BPA) containing plastic, and in particular, the leaching of BPA into food and beverages. In this context, it remains unclear whether and how exposure to BPA interferes with the developmental organization and adult activation of male sexual behavior by testosterone. We evaluated the developmental and adult exposure to oral BPA at doses equivalent to the no-observed-adverse effect-level (NOAEL, 5 mg/kg body weight/day) and tolerable daily intake (TDI, 50 mg/kg body weight/day) on mouse sexual behavior and the potential mechanisms underlying BPA effects.

Results:

Mice adult exposure to BPA reduced sexual motivation and performance at TDI dose only. Exposed males took longer to initiate mating and reach ejaculation despite normal olfactory chemoinvestigation. This deficiency was not restored by sexual experience and was associated with unchanged circulating levels of testosterone. By contrast, developmental exposure to BPA at TDI or NOAEL dose did not reduce sexual behavior or alter the neuroanatomical organization of the preoptic area. Disrupting the neural androgen receptor (AR) resulted in behavioral and neuroanatomical effects similar to those induced by adult exposure to TDI dose. Moreover, adult exposure of mutant males to BPA at TDI dose did not trigger additional alteration of sexual behavior, suggesting that BPA and neural AR mutation share a common mechanism of action.

Perspectives:

This shows, for the first time, that the neural circuitry underlying male sexual behavior is vulnerable to chronic adult exposure to low dose of BPA and suggests that BPA could act in vivo as an anti-androgenic compound.

Publication and collaboration

Picot M., Naule L., Marie-Luce C., Martini M., Raskin K., Grange-Messent V., Franceschini I., Keller M. & Mhaouty-Kodja S., 2014, Vulnerability of the neural circuitry underlying sexual behavior to chronic adult exposure to oral bisphenol A in male mice.  Endocrinology, 155, 502-512

In collaboration with Sakina Mhaouty Kodja group
Neurosciences Paris Seine
Equipe " Neuroplasticité des Comportements de Reproduction"
CNRS  UMR 8246, INSERM UMRS 1130, Université P. & M. Curie UM CR18
7 quai St Bernard, Bât A 3ème étage, Paris CEDEX 05