Poster, SOT 63rd Annual Meeting and ToxExpo, March 10–14, 2024, Salt Lake City, Utah.
Jun Woo Kim1, Ga Eun Kim2, Min-Seok Kim3, Ha Ryong Kim2,
1School of Pharmacy, Sungkyunkwan University, Suwon, Republic of Korea
2College of Pharmacy, Korea University, Sejong, Republic of Korea
3Korea Institute of Toxicology, Jeongeup, Republic of Korea
Didecyldimethylammonium chloride (DDAC) is an antimicrobial dialkyl-quaternary ammonium compound used in industrial and commercial products. Several animal studies suggest that inhaled DDAC triggers the respiratory toxicity including inflammation and fibrosis. In this study, we inferred DDAC-disease relationship using comparative toxicogenomics database. The DDAC aerosol was generated and exposed to human primary alveolar epithelial cells in Vitrocell system. The genome profile was obtained by next-generation sequencing. The differential expressed genes (DEGs) were determined with p value ≤ 0.05 and fold change 1.5 or greater. A comparative toxicogenomic dataset (CTD) analysis was applied to predict potential human respiratory diseases associated with exposure to DDAC. The cells were exposed to DDAC aerosol at a maximum concentration of 854 ng/cm2, at which cell viability decreased by 17%. A total of 1,996 DEGs, including 889 up- and 1,107 down-regulated genes, were identified. These DEGs were mainly enriched in cell-cell adhesion, mitochondrial translation, and so on. CTD analysis showed that DEGs were associated with respiratory diseases including asthma, fibrosis, and chronic obstructive pulmonary diseases. These results indicated that inhaled DDAC induced chronic inflammation and remodeling, ultimately causing respiratory diseases.
