Detailed Information

Cited 0 time in webofscience Cited 0 time in scopus
Metadata Downloads

Pulmonary inflammation and cellular responses following exposure to benzalkonium chloride: Potential impact of disrupted pulmonary surfactant homeostasis

Authors
Park, Eun-JungJin, Seung-WooKang, Min-SungYang, Mi-JinKim, Sung-HwanHan, Hyoung-YunKang, Jeong Won
Issue Date
1-4월-2022
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
Disinfectants; Benzalkonium chloride; Inflammation; Lamellar body-like structures; Autophagosome; Inhalation
Citation
TOXICOLOGY AND APPLIED PHARMACOLOGY, v.440
Indexed
SCIE
SCOPUS
Journal Title
TOXICOLOGY AND APPLIED PHARMACOLOGY
Volume
440
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/143425
DOI
10.1016/j.taap.2022.115930
ISSN
0041-008X
Abstract
Benzalkonium chloride (BKC) is a prototypical quaternary ammonium disinfectant. Previously, we suggested a no lethal dose level (0.005%) and an LD50 range (0.5-0.05%) of BKC following a single pharyngeal aspiration. Herein, we exposed BKC repeatedly by pharyngeal aspiration for 14 days (0.005 and 0.01%, female mice, total five times with interval of two days, 5 mice/group) and 28 days (0, 0.001, 0.005, and 0.01%, male and female mice, weekly, 16 mice/sex/group). Death following 14 days-repeated exposure did not occur. Meanwhile, chronic pathological lesions were observed in the lung tissues of mice exposed to BKC for 28 days. The total number of bronchial alveolar lavage cells increased, and pulmonary homeostasis of immunologic messenger molecules was disturbed. Following, we investigated BKC-induced cellular responses using human bronchial epithelial cells. The cytotoxicity increased rapidly with concentration. Lysosomal volume, NO production, and lipid peroxidation increased in BKC-treated cells, whereas intracellular ROS level decreased accompanying structural and functional damage of mitochondria. We also found that BKC affected the expression level of immune response, DNA damage, and amino acid biosynthesis-related molecules. More interestingly, lamellar body-and autophagosome-like structures were notably observed in cells exposed to BKC, and necrotic and apoptotic cell death were identified accompanying cell accumulation in the G2/M phase. Therefore, we suggest that repeated respiratory exposure of BKC causes pulmonary inflammation and lung tissue damage and that dead and damaged cells may contribute to the inflammatory response. In addition, the formation process of lamellar body-like structures may function as a key toxicity mechanism.
Files in This Item
There are no files associated with this item.
Appears in
Collections
Graduate School of Energy and Environment (KU-KIST GREEN SCHOOL) > Department of Energy and Environment > 1. Journal Articles

qrcode

Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.

Related Researcher

Researcher Kang, Jeong Won photo

Kang, Jeong Won
공과대학 (화공생명공학과)
Read more

Altmetrics

Total Views & Downloads

BROWSE