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STUDIES INTO THE MECHANISMS OF POTASSIUM BROMATE INDUCED THYROID CARCINOGENESIS
Citation:
Moore, T. M., L. M. Crosby, L. Yoon, M. P. Jokinen, AND A B. DeAngelo. STUDIES INTO THE MECHANISMS OF POTASSIUM BROMATE INDUCED THYROID CARCINOGENESIS. Presented at American Water Works Association Microbial/disinfection By-Products Effects Symposium, Lisle, IL, 3/24-26, 2001.
Description:
Studies into the Mechanisms of Potassium Bromate Induced Thyroid Carcinogenesis.
Potassium bromate (KBrO3) occurs in finished drinking water as a by-product of the ozonation disinfection process and has been found to induce thyroid follicular cell tumors in the rat after 100 weeks (DeAngelo et al., Toxicol. Pathol.,voI26:587-594, 1998). Little information exists on the mechanism(s) by which potassium bromate induces thyroid cancer . Thyroid hormone levels exert a significant effect on cellular metabolism, homeostasis, and central nervous system development. This study was conducted to examine the early effects of KBrO3 administered in the drinking water on the serum levels of thyroid stimulating hormone (TSH), triiodothyronine (T3), and thyroxin (T4), thyroid histopathology, follicular cell proliferation, and apoptosis. Male F344/N rats (28 days old) were exposed to 0,0.11 and 0.4 g/1 KBrO3 in the drinking water for 4 and 30 days. Serum TSH, T3, and T4 levels were measured by radioimmunoassay. KBrO3 treatment increased the concentration T3 (31.5 vs 17.6 ng/dl for control, p<0.05) and T4 (5.47 vs 3.51 ug/dl for control; p<0.05) at 30 days with no alterations of the TSH levels. The cell proliferation in animals exposed to KBrO3 did not differ from the untreated control values at 4 days, but was significantly elevated above the control value in the 0.4 g/L treatment group at 30 days. Increased apoptosis was observed in the high dose animals at both time periods (4 day TUNEL, 1.32% vs 1.05% for control, p
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