a National Center for Efficacy Evaluation of Respiratory Disease Product , Korea Institute of Toxicology , Jeongeup-si , Republic of Korea.
b Department of Human and Environmental Toxicology , University of Science & Technology , Daejeon , Republic of Korea.
J Toxicol Environ Health A. 2018;81(11):384-396. doi: 10.1080/15287394.2018.1451177. Epub 2018 Mar 28.
Cadmium (Cd) is a toxic metal present in tobacco smoke, air, food, and water. Inhalation is an important route of Cd exposure, and lungs are one of the main target organs for metal-induced toxicity. Cd inhalation is associated with an increased risk of pulmonary diseases. The present study aimed to assess the effects of repeated exposure to low-dose Cd in a mouse model of polyhexamethylene guanidine (PHMG)-induced lung fibrosis. Mice were grouped into the following groups: vehicle control (VC), PHMG, cadmium chloride (CdCl), and PHMG + CdCl. Animals in the PHMG group exhibited increased numbers of total cells and inflammatory cells in the bronchoalveolar lavage fluid (BALF) accompanied by inflammation and fibrosis in lung tissues. These parameters were exacerbated in mice in the PHMG + CdCl group. In contrast, mice in the CdCl group alone displayed only minimal inflammation in pulmonary tissue. Expression of inflammatory cytokines and fibrogenic mediators was significantly elevated in lungs of mice in the PHMG group compared with that VC. Further, expression of these cytokines and mediators was enhanced in pulmonary tissue in mice administered PHMG + CdCl. Data demonstrate that repeated exposure to low-dose Cd may enhance the development of PHMG-induced pulmonary fibrosis.
镉 (Cd) 是烟草烟雾、空气、食物和水中存在的一种有毒金属。吸入是接触镉的重要途径,肺部是金属诱导毒性的主要靶器官之一。吸入镉会增加患肺病的风险。本研究旨在评估在聚六亚甲基胍 (PHMG) 诱导的肺纤维化小鼠模型中反复低剂量接触 Cd 的影响。将小鼠分为以下几组:载体对照组 (VC)、PHMG、氯化镉 (CdCl) 和 PHMG + CdCl。PHMG 组的动物在支气管肺泡灌洗液 (BALF) 中显示总细胞和炎症细胞数量增加,伴有肺组织炎症和纤维化。在 PHMG + CdCl 组的小鼠中,这些参数加剧。相比之下,单独给予 CdCl 的小鼠仅在肺部组织中显示出轻微的炎症。与 VC 相比,PHMG 组小鼠肺部的炎症细胞因子和纤维生成介质的表达显著升高。此外,在给予 PHMG + CdCl 的小鼠的肺组织中,这些细胞因子和介质的表达增强。数据表明,反复低剂量接触 Cd 可能会增强 PHMG 诱导的肺纤维化的发展。