Journal
FOOD AND CHEMICAL TOXICOLOGY
Volume 98, Issue -, Pages 100-106Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2016.10.024
Keywords
Benomyl; ORMDL3; Reactive oxygen species; Human bronchial epithelial cells
Categories
Funding
- Cooperative Research Program for Agriculture Science & Technology Development (Project title: Development of alternative test for systemic toxicity and network analysis of toxicity parameters) of Rural Development Administration, Republic of Korea [PJ00995002]
- Research Institute for Veterinary Science, Seoul National University
- BK21 PLUS Program for Creative Veterinary Science Research
Ask authors/readers for more resources
The respiratory system is a major site of exposure route during pesticide use. Although pesticide exposure is associated with chronic respiratory diseases including asthma, the underlying pathophysiological mechanism remains to be elucidated. In this study, we investigated the in vitro effects of benomyl-induced ORMDL3 overexpression on the toxicological mechanism using the human bronchial epithelial cell line 16HBE14o-. Benomyl increased reactive oxygen species and Ca2+ levels, and asthma related ADAM33 and ORMDL3 expression in 16HBE14o- cells. Considering the change in Ca2+ level and protein expression, we focused on ORMDL3 to elucidate the mechanism of benomyl-induced asthma. Antioxidant treatment showed that benomyl-induced ORMDL3 and endoplasmic reticulum stress could be triggered by oxidative stress. Furthermore, ORMDL3 knockdown alleviated the effects of benomyl on intracellular Ca2+, and the expression of metalloproteinases, and proinflammatory cytokines involved in the pathogenesis of asthma. In conclusion, our results suggest that benomyl-induced ORMDL3 over expression via oxidative stress might be a mechanism involved in asthma. Moreover, antioxidants and alleviating mechanisms that reduce ORMDL3 levels could serve as promising therapeutic targets for pesticide-induced asthma. (C) 2016 Elsevier Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available