초록접수 현황
| 17F-133 | 포스터 발표 |
Chloromethylisothiazolinone and Methylisothiazolinone Induces Lung Epithelial Cell Damage.
Jooyeon Lee, Hanbyeol Lee, Soojin Jang, Jooyeon Se-Min Ryu, Sung-Min Park, Kyeong-Hak Lee, Sung-Joon Cho, Se-Ran Yang
Department of Thoracic and Cardiovascular Surgery, Kangwon National University Hospital, Kangwon National University College of Medicine, Gangwon-do, Republic of Korea
Purpose : Chloromethylisothiazolinone and methylisothiazolinone (CMIT/MIT) is a chemical mixture that commonly found in some cleaners such as dentifrice, germicide and shampoo at low concentration and had a water-soluble, high volatile properties and toxicity. The USA EPA registered CMIT/MIT as industry insecticide and announced that CMIT/MIT is the secondary inhalation toxic substance. Recently, in Korea, more than 400 victims had been suffered severe lung disease since they had used humidifier sterilizer that contained CMIT/MIT. Although it is unknown the risk factors of disinfectant, we investigated the cytotoxic effect of CMIT/MIT in the lungs of mice.
Methods : We treated CMIT/MIT (0, 12.5μM, 25μM, 50μM) for 24 hours in MLE-12 cells, which are mouse lung epithelial cells. Cell viability was analyzed by MTT assay after CMIT/MIT exposure. Then, we next determined the effect of CMIT/MIT exposure in animals, we intratracheally instilled CMIT/MIT (0, 0.5mg/kg, 1.5mg/kg) in C57BL/6 mouse.
Results : Exposure of CMIT/MIT induced cell death and inflammatory cytokine. CMIT/MIT exposed MLE-12 cells were increased the MAPK signaling pathway. In animal, administration of CMIT/MIT increased levels of inflammatory cytokine and induced infiltration of immune cells in mice lungs.
Conclusion : These findings suggest that CMIT/MIT exposure induce pulmonary damage in vitro and in vivo.
Methods : We treated CMIT/MIT (0, 12.5μM, 25μM, 50μM) for 24 hours in MLE-12 cells, which are mouse lung epithelial cells. Cell viability was analyzed by MTT assay after CMIT/MIT exposure. Then, we next determined the effect of CMIT/MIT exposure in animals, we intratracheally instilled CMIT/MIT (0, 0.5mg/kg, 1.5mg/kg) in C57BL/6 mouse.
Results : Exposure of CMIT/MIT induced cell death and inflammatory cytokine. CMIT/MIT exposed MLE-12 cells were increased the MAPK signaling pathway. In animal, administration of CMIT/MIT increased levels of inflammatory cytokine and induced infiltration of immune cells in mice lungs.
Conclusion : These findings suggest that CMIT/MIT exposure induce pulmonary damage in vitro and in vivo.
책임저자: Se-Ran Yang
Department of Thoracic and Cardiovascular Surgery, Kangwon National University Hospital, Kangwon National University College of Medicine, Gangwon-do, Republic of Korea
발표자: Jooyeon Lee, E-mail : 331joo@naver.com