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Triclosan exposure modulates estrogen-dependent responses in the rat.
Citation:
STOKER, T. E., R. L. COOPER, L. Zorrilla, AND E. K. GIBSON. Triclosan exposure modulates estrogen-dependent responses in the rat. Presented at Endocrine Society, Washington, DC, June 10 - 13, 2009.
Impact/Purpose:
This study was conducted to examine the estrogenic activity of the biocide triclosan
Description:
Triclosan (5-chloro-2-(2,4-dichlorophenoxy)phenol) is an antimicrobial that is currently found in a broad variety of personal care and sanitizing products, such as soaps, toothpaste and hair products. Triclosan (TCS) has been detected in human breast milk, blood samples and urine. These findings and the ability of TCS to bioaccumulate has led to recent concern for human health. In our previous studies, we have shown that TCS alters serum thyroid hormone concentrations and testosterone in male rats. In the current study, we examined the effects of triclosan in the weanling female rat and also tested the ability of TCS to interfere with receptor function. First, we evaluated the potential estrogenicity of triclosan using the immature rat uterotrophic assay. Weanling female rats were given oral doses of either TCS (from 1.17 mg/kg to 37.5) or 3 ug/kg ethinyl estradiol (EE) or TCS in combination with EE. Uterine weight was increased in the EE group as compared to the control, but was not affected by TCS alone. However, there was a significant dose-dependent increase in the group co-treated with EE and TCS (≥ 4.69 mg/kg) as compared to EE alone, indicating a potentiation of the estrogen response on uterine weight (NOEL=2.34 mg/kg). In addition, this result was correlated with estrogen-induced changes in uterine histology. Next, we tested the ability of TCS to alter a cell-based estrogen receptor (ER) transcriptional activation (TA) assay. TCS concentrations of .003 to 10μM were evaluated and TCS alone did not have agonistic or antagonistic activity in this assy. In addition, co-incubations of TCS and various concentrations of estradiol resulted in a response comparable to estradiol alone, indicating that the parent compound does not potentiate ER TA. In conclusion, there appears to be several effects of TCS on estrogen-mediated uterine response in the weanling female rat. Based on the ER TA results, it is possible that one of the metabolites of TCS may be responsible for the observed effect in vivo. Current studies are evaluating other potential modes of action for the effect. This abstract does not reflect EPA policy.