Paulus Brian F, Bazar Matthew A, Salice Christopher J, Mattie David R, Major Michael A
Directorate of Toxicology, Health Effects Research Program, U.S. Army Center for Health Promotion and Preventive Medicine, Aberdeen Proving Ground, Maryland 21010, USA.
J Toxicol Environ Health A. 2007 Jul;70(13):1142-9. doi: 10.1080/15287390701252741.
Perchlorate-induced inhibition of thyroidal iodide uptake was measured in normal and iodine-deficient female Sprague-Dawley rats. Rats that were made iodine-deficient by long-term restriction of iodine in the diet absorbed a gavage dose of 131I to the thyroid in proportionally greater amounts than rats fed a normal diet. Furthermore, the iodine-deficient rats maintained their high rates of absorption even when challenged by levels of perchlorate in their drinking water sufficient to produce pronounced inhibition of 131I uptake in rats fed a normal diet. Every dose of perchlorate used in this study (1.1, 5.6, and 28 mg/L) produced significant inhibition of iodide uptake in normally fed rats, but only the highest level of perchlorate (28 mg/L) significantly inhibited thyroidal uptake of 131I in the iodine-deficient rats. Taken together, these results demonstrate that iodide-deficient animals exhibit increased resistance to the inhibition of iodine absorption resulting from perchlorate exposure.
在正常和缺碘的雌性斯普拉格-道利大鼠中,测定了高氯酸盐对甲状腺碘摄取的抑制作用。通过长期限制饮食中的碘而造成缺碘的大鼠,相对于喂食正常饮食的大鼠,经口灌胃给予的131I按比例更多地被甲状腺吸收。此外,即使饮用水中的高氯酸盐水平足以对喂食正常饮食的大鼠产生明显的131I摄取抑制作用,缺碘大鼠仍保持其高吸收率。本研究中使用的每一个高氯酸盐剂量(1.1、5.6和28mg/L)都对正常喂食的大鼠的碘摄取产生了显著抑制作用,但只有最高水平的高氯酸盐(28mg/L)显著抑制了缺碘大鼠的甲状腺对131I的摄取。综上所述,这些结果表明,缺碘动物对高氯酸盐暴露导致的碘吸收抑制表现出增强的抵抗力。