AI Article Synopsis
- Third-hand smoke (THS) is harmful residual smoke that remains on surfaces and can negatively affect respiratory health, especially in individuals with preexisting conditions.
- The study investigated how THS causes respiratory toxicity through mechanisms like increased reactive oxygen species (ROS), cytotoxicity, and inflammation in human airway cells.
- Findings indicated that THS leads to oxidative stress, as evidenced by increased levels of malondialdehyde and interleukin-6, along with decreased antioxidant activity, potentially exacerbating respiratory diseases.
Article 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 HO-induced oxidative stress model of human airway epithelia .
Materials And Methods: THS extracted from terrycloth exposed to 3R4F cigarettes was assessed 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay to identify cytotoxicity. The reactive oxygen species (ROS) level was determined 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 enzyme-linked immunosorbent assay.
Results: THS 50% () with significant cytotoxicity in A549 cells upregulated intracellular ROS levels a right-shifted fluorescence intensity of DCFDA compared with the control ( < 0.05), which was also amplified with HO co-treatment. MDA levels remarkably increased with THS ( < 0.05). Both THS and THS + HO led to notable GSH depletion, increased CAT activity, and increased IL-6 levels, which were attenuated by the negative control (N-acetylcysteine, 1 mM) ( < 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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11600328 | PMC |
| http://dx.doi.org/10.4274/tjps.galenos.2024.36153 | DOI Listing |
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