You are here:
The Effects of Oral Triclosan Exposure on Reproductive Endpoints in the Female Wistar Rat.
Citation:
STOKER, T. E. The Effects of Oral Triclosan Exposure on Reproductive Endpoints in the Female Wistar Rat. Presented at Society for the Study of Reproduction, Portland, OR, July 31 - August 04, 2011.
Impact/Purpose:
Measurable amounts of TCS have been detected in human blood, urine, and breast milk. Recently, we and others have demonstrated that TCS is an endocrine disruptor because TCS treatment decreases thyroxine and testosterone in rats, thus raising new concerns that this compound may adversely affect human health.
Description:
Triclosan (TCS) is an antimicrobial agent commonly found in household personal care and consumer products such as soaps, toothpaste and kitchen utensils. Measurable amounts of TCS have been detected in human blood, urine, and breast milk. Recently, we and others have demonstrated that TCS is an endocrine disruptor because TCS treatment decreases thyroxine and testosterone in rats, thus raising new concerns that this compound may adversely affect human health. We also reported that acute oral exposures (PND 19-21) to TCS alone in weanling rats did not alter uterine growth, however, combining TCS (≥4 mg/kg) exposure and ethinyl estradiol (EE) potentiated the effects of EE on uterine growth (i.e., increased uterine weight and epithelial cell height) in a dose-dependent manner. To further characterize potential adverse effects associated with TCS action on estrogen- mediated events, here we examined the effect of an extended (21d) oral exposure to TCS (9-150 mg/kg) in the intact juvenile female rat during a period in which they begin to secrete endogenous estrogens (PND 21-41). We found that 150 mg/kg of TCS advanced the age of vaginal opening and increased uterine weight, indicative of an estrogenic effect. Histological evaluation ofthese uteri revealed an increase in glandular cell height (representative of estrogenic stimulation) compared to controls. Furthermore, we also evaluated the effects of a chronic (120d) exposure to TCS on the estrous cycle in adult female rats, as well as other reproductive endpoints, using EE (1 ug/kg p.o.) as a positive control. Results show that EE and the higher doses of TCS altered normal estrous cyclicity. Identifying the mechanism(s) through which TCS enhances EE activity (e.g., altering the estrogen receptor or estrogen clearance) will be central to the proper characterization of the adverse action of this antimicrobial in the female rat. This abstract does not necessarily reflect us. EPA policy. This research was supported in part by the NCSU-EPA Cooperative Training in Environmental Sciences Research Program.