Perfluorooctane Sulfonate-Induced Thyroid Hormone Disruption in the Rat

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Title: Perfluorooctane Sulfonate-Induced Thyroid Hormone Disruption in the Rat
Author: Thibodeaux, Julie Rene
Advisors: Jill Barnes, Committee Co-Chair
Christopher Lau, Committee Co-Chair
John M. Rogers, Committee Member
Abstract: Perfluorooctane sulfonate (PFOS) is a perfluoroalkyl acid that has unique surfactant properties and is used widely in industrial and household products. Furthermore, PFOS is an environmentally persistent compound, and its presence has been detected in both humans and wildlife. The maternal and developmental toxicities of PFOS were evaluated in Sprague-Dawley rats given 1, 2, 3, 5, or 10 mg/kg PFOS daily from gestational day (GD) 2 to GD 20. Controls received 0.5% Tween 20 vehicle (1 ml/kg). Serum thyroxine (T4) and triiodothyronine (T3) in the PFOS-treated dams were significantly reduced as early as one week after chemical exposure, although no feedback response of thyroid stimulating hormone (TSH) was observed. The effects of sub-chronic exposure to PFOS (3 mg/kg/day for eight days) on thyroid hormone economy are further characterized in adult male rats, and the thyrotoxic effects of PFOS are compared to propylthiouracil (PTU), a classic goitrogen. This work substantiates the endocrine disrupting effects of PFOS, but fails to provide evidence for its physiological consequences in comparison to PTU based on two biomarkers of hypothyroidism: myocardial beta-adrenergic receptor density and hepatic malic enzyme activity. Furthermore, in vitro static incubation of the pituitary is used to investigate the observed lack of response of the hypothalamic-pituitary-thyroid axis. PFOS does not significantly alter thyrotropin releasing hormone (TRH) induced secretion of TSH from the pituitary. Therefore, it is not likely that PFOS-induced changes in circulating thyroid hormones are due to a disruption at the level of the pituitary.
Date: 2005-06-27
Degree: MS
Discipline: Comparative Biomedical Sciences
URI: http://www.lib.ncsu.edu/resolver/1840.16/1549


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