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Keisuke Kawai,^1,2 Takehiro Nozaki,¹ Hiroaki Nishikata,¹ Shuji Aou,^2,3 Masato Takii,¹ and Chiharu Kubo^1,2

¹Department of Psychosomatic Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan; ²Core Research for Evolutional Science and Technology, Japan Science and Technology, Kawaguchi, Japan; ³Department of Integrative Physiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan

Abstract

The relationship between exposure to endocrine-disrupting chemicals (EDs) and risk to reproductive organs is well documented, but the influence of EDs on behavioral development has not been studied. In this study we evaluated the effect of fetal exposure to bisphenol A, which mimics estrogenic activity, on aggressive behavior and hormonal change in male mice. On gestation days 11-17, female mice were fed bisphenol A at 2 ng/g or 20 ng/g of body weight (environmentally relevant concentration) . Aggression rating and blood sampling of the offspring were done at 8, 12, and 16 weeks of age. Aggression scores increased significantly (p < 0.01) at 8 weeks of age in male mice exposed to bisphenol A at both the 2 ng/g and 20 ng/g concentrations compared with a control group, but no difference was found after 12 weeks. Relative testis weight (per gram of body weight) was significantly lower at 8 and 12 weeks in mice treated with 2 ng/g than in controls (p < 0.05) and was significantly lower at 12 weeks in mice treated with 20 ng/g than in controls (p < 0.01) . The serum testosterone concentration in treated mice was not significantly different from that in controls. These results demonstrate that bisphenol A temporarily activated aggressive behavior in mice at 8 weeks of age and that low doses of bisphenol A interfered with the normal development of reproductive organs. The mechanism activating this aggressive behavior was not elevated testosterone concentration. Key words: aggression, behavior, bisphenol A, mice, sexually mature, testosterone. Environ Health Perspect 111:175-178 (2003) . doi:10.1289/ehp.5440 available via http://dx.doi.org/ [Online 1 October 2002]