Third-Hand Smoke Exacerbates H<sub>2</sub>O<sub>2</sub>-Driven Airway Responses in A549 Cells
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Original Article
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Third-Hand Smoke Exacerbates H2O2-Driven Airway Responses in A549 Cells

1. Acıbadem Mehmet Ali Aydınlar University Faculty of Pharmacy Department of Toxicology, İstanbul, Türkiye
2. Yeditepe University Faculty of Pharmacy Department of Toxicology, İstanbul, Türkiye
3. Acıbadem Mehmet Ali Aydınlar University Faculty of Pharmacy Department of Pharmaceutical Chemistry, İstanbul, Türkiye
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Received Date: 13.09.2023
Accepted Date: 12.01.2024
Online Date: 04.10.2024
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ABSTRACT

Objectives: Third-hand smoke (THS) is residual smoke after extinguishing a cigarette and adhering to surfaces. Re-emission into the air also makes THS a health concern for those who suffer from respiratory diseases. The present study aimed to elucidate the mechanistic pathways involved in THS-induced respiratory toxicity and the accelerative potential of THS in an H2O2-induced oxidative stress model of human airway epithelia in vitro.

Materials and Methods: THS extracted from terrycloth exposed to 3R4F cigarettes was assessed via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay to identify cytotoxicity. The reactive oxygen species (ROS) level was determined via 2,7-dichlorofluorescein diacetate (DCFDA) fluorescence intensity in a flow cytometer, and glutathione (GSH), malondialdehyde (MDA), and catalase (CAT) activity were assessed spectrophotometrically. Interleukin-6 (IL-6) level was measured via enzyme-linked immunosorbent assay.

Results: THS 50% (v/v) with significant cytotoxicity in A549 cells upregulated intracellular ROS levels via a right-shifted fluorescence intensity of DCFDA compared with the control (p < 0.05), which was also amplified with H2O2 co-treatment. MDA levels remarkably increased with THS (p < 0.05). Both THS and THS + H2O2 led to notable GSH depletion, increased CAT activity, and increased IL-6 levels, which were attenuated by the negative control (N-acetylcysteine, 1 mM) (p < 0.05).

Conclusion: The induction of oxidative stress may be an important event in THS-induced airway toxicity that may contribute to the progression of respiratory diseases.