Customer Publication

Chlorine exposure induces Caspase-3 independent cell death in human lung epithelial cells

Authors: T. Karlsson et al.

Journal: Toxicology in Vitro (2022)

Institution: Swedish Defence Research Agency

Research Areas: Toxicology

Cell Lines: A549 (Lung epithelial cell)

Summary: Chlorine (Cl2) is a common toxic industrial gas and this study aimed to investigate the in vitro cellular effects after Cl2 exposure of human A549 lung epithelial cells and the possible treatment of the anti-inflammatory antioxidant N-acetyl cysteine (NAC). Exposure of A549 cells to Cl2 (100–1000 ppm) in the cell medium induced cell damage and toxicity within 1 h in a dose-dependent manner. The results showed that 250 ppm Cl2 increased cell death and the formation of apoptotic-like bodies, while 500 ppm Cl2 exposure resulted in predominantly necrotic death. Pre-treatment with NAC was efficient to prevent cell damage at lower Cl2 concentrations in part by averting the formation of apoptotic-like bodies and increasing the expression of the anti-apoptotic proteins clusterin and phosphorylated tumor protein p53(S46). The study showed that Cl2 induced cell death by a possibly caspase-independent mechanism. HoloMonitor m4 was used for cell morphology, cell migration and cell proliferation studies.

Keywords: HoloMonitor M4, Cell morphology, Cell migration, Cell proliferation, Chlorine, Caspase-3, N-acetyl cysteine, Human lung epithelial cells, Cell injury, Cell death

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