Exposure to endocrine-disrupting chemicals may adversely affect animals, particularly during development. Tris(1,3-dichloroisopropyl) phosphate (TDCIPP) is an organophosphate with anti-androgen function in vitro that is present in indoor dust at relatively high concentrations. In male rats, androgens are necessary for the development of reproductive organs, as well as the endocrine and central nervous systems. However, we currently do not know the exact effects of TDCIPP exposure through suckling on subsequent reproductive behavior in males. Here, we show that TDCIPP exposure (25-250 mg kg-1 via oral administration over 28 consecutive days post-birth) suppressed male sexual behavior and reduced testes size. These changes were dose-dependent and appeared first in adults rather than in juveniles. These results demonstrate that TDCIPP exposure led to normal body growth and appearance in juveniles, but disrupted the endocrine system and physiology in adults. Therefore, assays should be performed using adult animals to ensure accuracy, and to confirm the influence of chemical substances given during early mammalian life.
Anxiety disorder risk is influenced by both adverse environmental factors and genetic background. We previously described high-avoidance animal (HAA) and low-avoidance animal (LAA) strains of male Hatano rats that may provide robust models for assessing interactions between genetic background and environment driving anxiety disorder pathogenesis. We examined the potential of environmental enrichment (EE), a non-pharmacological approach, to suppress trait anxiety disorders by comparing anxiety-related behaviors and physiological metrics between HAA and LAA lines exposed to EE or standard housing. At 4 weeks of age, 10-12 male rats from each strain were assigned to EE or standard conditions. EE for 4-5 weeks significantly (p = 0.0002 by Tukey-Kramer's test) reduced anxiety-related behaviors in LAAs in the elevated plus maze test, but had no similar anxiolytic effect in HAAs. In contrast, EE for 11 weeks significantly (p = 0.0072 by Tukey-Kramer's test) reduced passive avoidance memory retention in HAAs, but not in LAAs. Real-time quantitative PCR revealed upregulated expression of Bdnf exons 1, 3, and 4 in the hippocampus of LAAs following EE, while the same treatment increased the expression of Bdnf exon 3 in the hippocampus of HAAs. Alternatively, EE did not alter mRNA expression levels of the BDNF receptor TrkB and the glucocorticoid receptor in hippocampus, or influence plasma corticosterone, prolactin, and testosterone concentrations. These findings have potential clinical implications for anxiety disorders, suggesting that effects of EE may vary depending on an individual's genetic background and underlying biological characteristics.