Meeting Abstract

P1.83  Wednesday, Jan. 4  The estrogen-disrupting compounds bisphenol-A (BPA) and atrazine inhibit thymus gland growth in amphibian (Xenopus laevis) tadpoles PRIYAMVADA, L.; GARCIA, J.*; HECKMAN, K.; SCHREIBER, A.M.; St. Lawrence Univ.; St. Lawrence Univ.; St. Lawrence Univ.; St. Lawrence Univ. aschreiber@stlawu.edu

High levels of endogenously-produced or exogenously-administered estrogen are known to cause the thymus to atrophy in vertebrates, presumably via interaction with nuclear-localized estrogen receptors. The herbicide, atrazine, has been shown to increase estrogen synthesis by inducing the cytochrome p450 aromatase enzyme, and has also been shown to cause thymic involution in mammals and in adult frogs. The polycarbonate plastic monomer, BPA, is a well-known estrogen receptor agonist that has been shown to inhibit thymus development in birds and mammals. Here we show that treatment of young tadpoles (7 days-post fertilization; Nieuwkoop and Faber stage 50) for 5-7 days with BPA (10 uM), atrazine (200 uM), estradiol (10 uM), or dexamethasone (2 uM) significantly reduces thymus gland size by 11%, 20%, 35%, and 67%, respectively. Differences in thymus size were independent of tadpole somatic size, which did not differ among treatments. In contrast, treatment with thyroid hormone (7 uM triiodothyronine, T3) caused a significant increase (20%) in thymus gland size. Interestingly, compared to tadpoles treated with estradiol alone, concurrent treatment with estradiol (10 uM) + fulvestrant (25 uM; an estrogen receptor antagonist) produced tadpoles with significantly larger (30%) thymus glands. However, the thymuses of estradiol+fulvestrant treated tadpoles were still significantly smaller (23%) compared with untreated controls, suggesting that some of the effects of estradiol and its endocrine-disrupting agonists may circumvent the estrogen receptor pathway.