Huffman L J, Beighley C M, Frazer D G, McKinney W G, Porter D W
Health Effects Laboratory Division, National Institute for Occupational Safety and Health, M/S 2015, 1095 Willowdale Road, Morgantown, WV 26505, USA.
Toxicology. 2006 Aug 15;225(2-3):119-27. doi: 10.1016/j.tox.2006.05.008. Epub 2006 May 20.
Results from previous studies indicate that hyperthyroidism increases the risk of ozone-induced lung toxicity. This observation raised the possibility that pulmonary damage from other oxidant substances might be greater in a hyperthyroid state. To address this hypothesis, pulmonary responses to crystalline silica, a particulate with oxidant properties, were evaluated in normal or hyperthyroid adult male rats. To induce a hyperthyroid condition, time-release pellets containing thyroxine were implanted subcutaneously; control rats received placebo pellets. After 7 days, the animals were exposed to saline or silica (0.1mg/100g BW or 1.0mg/100g BW) by intratracheal instillation. Following silica treatment, there was a dose-related increase in bronchoalveolar lavage (BAL) albumin levels and neutrophil numbers. However, the effects of silica were similar in both normal and hyperthyroid rats. These findings were confirmed and contrasted with those regarding ozone (1ppm, 4h inhalation) in a subsequent experiment. The results indicated that, although exposure to either ozone or silica resulted in increases in BAL albumin levels and neutrophil numbers, only responses to ozone were enhanced in hyperthyroid rats. These findings suggest that specificity exists in regards to the modulation of oxidant-induced lung damage and inflammation by thyroid hormones.
以往研究结果表明,甲状腺功能亢进会增加臭氧诱导的肺毒性风险。这一观察结果引发了一种可能性,即甲状腺功能亢进状态下,其他氧化物质对肺部的损害可能更大。为了验证这一假设,研究人员评估了正常或甲状腺功能亢进的成年雄性大鼠对具有氧化特性的颗粒状结晶二氧化硅的肺部反应。为诱导甲状腺功能亢进状态,皮下植入含甲状腺素的缓释微丸;对照大鼠接受安慰剂微丸。7天后,通过气管内滴注使动物接触生理盐水或二氧化硅(0.1mg/100g体重或1.0mg/100g体重)。二氧化硅处理后,支气管肺泡灌洗(BAL)白蛋白水平和中性粒细胞数量呈剂量相关增加。然而,正常大鼠和甲状腺功能亢进大鼠对二氧化硅的反应相似。这些发现随后在一项实验中得到证实,并与臭氧(1ppm,吸入4小时)的相关发现进行了对比。结果表明,尽管接触臭氧或二氧化硅都会导致BAL白蛋白水平和中性粒细胞数量增加,但只有甲状腺功能亢进大鼠对臭氧的反应增强。这些发现表明,甲状腺激素对氧化诱导的肺损伤和炎症的调节存在特异性。