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    The Effects of Individual Components of E-Cigarettes on Ion Transport and Airway Surface Liquid Height in Human Bronchial Epithelial Cells
    (Mdpi, 2025) Beyazcicek, Ozge; Tarran, Robert; Ozmerdivenli, Recep; Beyazcicek, Ersin
    Background and Objectives: The rising popularity of new-generation electronic cigarettes (e-cig) like JUUL necessitates a better understanding of their impact on respiratory and other body systems, as the effects of JUUL's components remain unclear. This study aimed to investigate the effects of JUUL components on ion channels and airway surface liquid (ASL) height in human bronchial epithelial cells (HBECs). Furthermore, the cytotoxic effects of these components were investigated in human embryonic kidney 293T (HEK293T) cells. Materials and Methods: The components tested included nicotine salt (NicSalt), benzoic acid (BA), sodium hydrogen tartrate (NaTar), propylene glycol/vegetable glycerin (PG/VG), freebase nicotine (FBNic) and nicotine salt+benzoic acid (NicSalt+BA). Each component was prepared at 100 mu M, and HBECs were exposed for 24 h to measure ASL height, short-circuit current (Isc), and transepithelial electrical resistance (TEER). Results: Initial exposure (0 h) to these substances did not significantly alter ASL height. However, after 2 h, FBNic-treated HBECs exhibited a significant reduction in ASL height compared to NicSalt and other tested substances, with the most pronounced decrease observed at the 6th hour. This effect persisted over prolonged exposure, suggesting a cumulative impact on airway hydration and epithelial function. Additionally, adenosine administration did not induce a significant increase in ASL height. NicSalt, BA, and FBNic were found to disrupt ion balance in HBECs, affecting ion channels and ASL homeostasis while significantly decreasing TEER. In terms of cytotoxicity, NicSalt, and benzoic acid demonstrated minimal cytotoxicity at low concentrations, whereas FBNic showed significantly higher cytotoxicity at moderate levels. Conclusions: In conclusion, this study highlights that e-cigarette components can disrupt airway surface liquid homeostasis by affecting ion channel activity, compromise epithelial barrier integrity by reducing transepithelial electrical resistance, and emphasize the importance of their cytotoxic effects.
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    Protective Mechanisms of EGCG in Mitigating Oxidative Stress and Liver Toxicity From Cigarette Smoke-Induced Damage
    (Wiley, 2025) Agan, Kagan; Demir, Serif; Ozmerdivenli, Recep; Agan, Aydan Fulden; Akin, Ali Tugrul; Alpay, Merve; Beyazcicek, Ozge
    Exposure to cigarette smoke leads to an increase in oxidative stress within the body, resulting in both an elevated oxidant burden and a compromised antioxidant defense system. This imbalance creates a significant risk factor for various diseases by promoting cellular damage, inflammation, and toxicity. The oxidants present in cigarette smoke are considered the primary contributors to these pathological conditions. Supporting the antioxidant system with specific bioactive compounds may help mitigate the toxic effects caused by cigarette smoke. In this study, the effects of EGCG pre-administration on the antioxidant system were evaluated under both acute and chronic exposure conditions to cigarette smoke. Different doses of EGCG were administered to determine its potential role in oxidative stress regulation, and histopathological examinations and antioxidant enzyme levels were assessed. The findings demonstrated that while acute EGCG administration did not significantly improve antioxidant enzyme activity, chronic administration of EGCG at a dose of 50 mg/kg effectively increased antioxidant enzyme production, reduced oxidative stress, and liver injury. In the presence of cigarette smoke, EGCG contributed to the stabilization of oxidative stress markers. However, chronic EGCG administration in the absence of oxidative stressors requires further investigation to assess its impact on other organs. EGCG appears to be a promising candidate for alleviating the adverse effects of external oxidant exposure and mitigating oxidative stress. However, its long-term application and potential side effects in different physiological conditions should be explored further examinations. Although acute EGCG application did not enhance antioxidant enzyme levels, it unexpectedly elevated oxidative stress, emphasizing the need for more comprehensive studies to clarify its mechanisms and optimize its usage. We further identify the principal underlying mechanisms involved in this process.