Gordon C J, Becker P, Padnos B
Neurotoxicology Division, National Health and Environmental Effects Research Laboratory, United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA.
Am J Physiol Regul Integr Comp Physiol. 2000 Dec;279(6):R2066-71. doi: 10.1152/ajpregu.2000.279.6.R2066.
How borderline impairment of thyroid function can affect thermoregulation is an important issue because of the antithyroidal properties of a many environmental toxicants. This study compared the efficacy of heat and cold stress to identify thermoregulatory deficits in rats subjected to borderline and overt hypothyroidism via subchronic exposure to propylthiouracil (PTU). After 3 wk of exposure to PTU in the drinking water (0, 2.5, 5, 10, and 25 mg/l), rats were subjected to a heat stress challenge (34 degrees C for 2.5 h). After one more week of PTU treatment, the same rats were subjected to a cold stress challenge (7 degrees C for 2.5 h). Core temperature (T(c)) was monitored by radiotelemetry. Baseline T(c) during the light phase was reduced by treatment with 25 mg/l PTU. The rate of rise and overall increase in T(c) during heat stress was attenuated by PTU doses of 10 and 25 mg/l. Cold stress resulted in a 1.0 degrees C increase in T(c) regardless of PTU treatment. The rate of rise in T(c) during the cold stress challenge was similar in all PTU treatment groups. There was a dose-related decrease in serum thyroxine (T(4)) at PTU doses >/=5 mg/l. Serum triiodothyronine (T(3)) was reduced at PTU doses of 5 and 25 mg/l. Serum thyroid-stimulating hormone (TSH) was marginally elevated by PTU treatment. Overall, heat stress was more effective than cold stress for detecting a thermoregulatory deficit in borderline (i.e., 10 mg/l PTU) and overtly hypothyroid rats (i.e., 25 mg/l PTU). A significant thermoregulatory deficit is manifested with a 78% decrease in serum T(4). A thermoregulatory deficit is more correlated with a reduction in serum T(4) compared with T(3). Serum levels of TSH are unrelated to thermoregulatory response to heat and cold stress.
鉴于许多环境毒物具有抗甲状腺特性，甲状腺功能的临界损害如何影响体温调节是一个重要问题。本研究比较了热应激和冷应激对通过亚慢性给予丙硫氧嘧啶（PTU）导致临界和明显甲状腺功能减退大鼠体温调节缺陷的识别效果。在饮用水中暴露于PTU 3周（0、2.5、5、10和25 mg/l）后，大鼠接受热应激挑战（34℃，持续2.5小时）。在PTU治疗再持续一周后，相同的大鼠接受冷应激挑战（7℃，持续2.5小时）。通过无线电遥测监测核心体温（T(c)）。用25 mg/l PTU治疗可降低光照期的基线T(c)。10和25 mg/l的PTU剂量可减弱热应激期间T(c)的上升速率和总体升高幅度。无论PTU治疗如何，冷应激导致T(c)升高1.0℃。在所有PTU治疗组中，冷应激挑战期间T(c)的上升速率相似。PTU剂量≥5 mg/l时，血清甲状腺素（T(4)）呈剂量相关下降。5和25 mg/l的PTU剂量可降低血清三碘甲状腺原氨酸（T(3)）。PTU治疗使血清促甲状腺激素（TSH）略有升高。总体而言，热应激在检测临界（即10 mg/l PTU）和明显甲状腺功能减退大鼠（即25 mg/l PTU）的体温调节缺陷方面比冷应激更有效。血清T(4)下降78%时表现出明显的体温调节缺陷。与T(3)相比，体温调节缺陷与血清T(4)的降低更相关。血清TSH水平与对热应激和冷应激的体温调节反应无关。
