Adams J D, Laegreid W W, Huijzer J C, Hayman C, Yost G S
Pharmacology/Toxicology Program, Washington State University, Pullman 99164.
Res Commun Chem Pathol Pharmacol. 1988 Jun;60(3):323-36.
Light and electron microscopic studies were performed to assess the pathology induced by 3-methylindole (3MI) in Sprague-Dawley rats and Swiss-Webster mice. Rats have not been established as a susceptible species to 3MI-induced pulmonary damage, whereas mice are known to be a good model for this pneumotoxicity. Therefore, mice were used as a comparison species for pneumotoxicity studies in the rat. Rats were as susceptible to 3MI-mediated toxicity as mice. The loss of Clara cells in the bronchiolar epithelium was the major pulmonary lesion in both species. Alveolar cells in the lungs of either species were not damaged. The only other lesion in the rat was that the nasal epithelium was totally eroded in caudal areas of the sinuses. Glutathione was depleted by 3MI in pulmonary tissues of mice and rats. Maximal depletion (53% of control values) occurred in rat lung. This work demonstrates that both rodent species are susceptible to 3MI-induced pulmonary damage.
进行了光镜和电镜研究,以评估3-甲基吲哚(3MI)对斯普拉格-道利大鼠和瑞士-韦伯斯特小鼠造成的病理变化。大鼠尚未被确定为对3MI诱导的肺损伤敏感的物种,而小鼠已知是这种肺毒性的良好模型。因此,将小鼠用作大鼠肺毒性研究的对照物种。大鼠对3MI介导的毒性与小鼠一样敏感。细支气管上皮中克拉拉细胞的丧失是这两个物种的主要肺部病变。两个物种肺中的肺泡细胞均未受损。大鼠的唯一其他病变是鼻窦尾部区域的鼻上皮完全糜烂。3MI使小鼠和大鼠肺组织中的谷胱甘肽耗竭。大鼠肺中出现最大耗竭(对照值的53%)。这项工作表明,两种啮齿动物物种均易受3MI诱导的肺损伤。