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Effects of Chronic Exposure to Triclosan on Reproductive and Thyroid Endpoints in the Adult Wistar Female Rat
Citation:
Louis, G., D. Hallinger, J. Braxton, A. Kamel, AND T. Stoker. Effects of Chronic Exposure to Triclosan on Reproductive and Thyroid Endpoints in the Adult Wistar Female Rat. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH - PART A: CURRENT ISSUES. Taylor & Francis, Inc., Philadelphia, PA, 80(4):236-249, (2017).
Impact/Purpose:
This manuscript describes the effects of a long term exposure to triclosan on the reproductive and thyroid axis. This was in response to the need to examine the potential of triclosan to alter the timing of reproductive senescence in the rat based on earlier observations of an enhancement of the estrogen induced uterine response. In addition, information on the long term exposure on thyroid axis was important to determine if TSH or thyroid histopathology would be altered, as no effects were observed on these parameters in the shorter exposure studies. No significant effects were observed on the reproductive portion of the study and similar changes in the thyroid axis as shown in earlier work.
Description:
Triclosan (TCS), an antibacterial agent found in many consumer products, has been shown to be an endocrine disruptor in the rat. We reported previously that TCS treatment to female rats advanced puberty and potentiated the effect of ethinyl estradiol (EE) on uterine growth when EE and TCS were co-administered prior to weaning. In the female pubertal study, we also observed a decrease in serum thyroxine (T4) concentrations with no significant change in serum thyroid stimulating hormone (TSH) or triiodothyronine (T3) levels. The purpose of the present study was to further characterize the effect of triclosan on the reproductive and thyroid axes of the female rat using a chronic exposure regimen. Female Wistar rats were exposed to vehicle control, EE (1.0 μg/kg), or TCS (2.3, 4.69, 9.375, and 37.5 mg/ kg) for approximately eight months (postnatal days 110-346). Estrous cyclicity was assessed by vaginal cytology throughout the dosing period. Although a divergent pattern of reproductive senescence appeared to emerge from 5 to 11 months of age between the controls and the EE females, no significant difference in cyclicity was observed between triclosan-treated and control females. A greater number of control females displayed persistent diestrus (PD) by the termination of the study, whereas animals treated with the positive control (EE) were predominately persistent estrus (PE) at this time. When thyroid status was assessed at the end of dosing, T4 was significantly decreased in TCS 9.375 and 37.5 mg/kg groups, but none of the TCS exposures resulted in significant changes in TSH, thyroid tissue weight or thyroid histology as compared to controls. The results of this study demonstrate that a long term exposure to TCS does not significantly alter estrous cyclicity or timing of reproductive senescence in females. However, this study did find a suppression of T4 at a lower dose of TCS than previously observed in the rat and reconfirmed that there was no concomitant increase in TSH or change in thyroid weight or histopathology.
