Abstract
Smoking, a major behavioral health burden, causes preventable and premature deaths globally. Nicotine, the addictive component present in tobacco products and Electronic cigarettes (E-cigarettes, vape), can bind to nicotinic acetylcholine receptors in the brain to trigger a dopamine release that reinforces smoking. Despite the widespread usage of nicotine, its mechanisms of toxicity, particularly in e-cigarettes, are poorly understood. Using Drosophila melanogaster as a model organism, this study aims to investigate the mechanism of the toxicity of nicotine and vape. Behavioral parameters, oxidative stress indicators, mRNA expression levels of Dopamine 1- receptor 1 (Dop1R1), Acetyl-coenzyme A synthetase (AcCoAs), and apoptotic proteins were assessed in the flies after a 5-day exposure to varying concentrations of nicotine (0.15, 0.25, and 0.35 mg/mL diet) and vape (0.06, 0.08, and 0.12 mg/mL diet). Furthermore, Gas Chromatography-Mass Spectrometry (GC/MS) and Gas Chromatography-Flame Ionization Detection (GC/FID) analyzes were conducted to gain more insight on the composition of the vape used in study. Findings indicate that both nicotine and vape exposure significantly reduced lifespan, impaired locomotor activity, and disrupted sleep patterns. Notably, nicotine exposure stimulated Dop1R1 transcription and altered Acetyl-CoA gene expression, impacting the viability and behavior of the flies. Elevated levels of reactive oxygen biomarkers were observed, contributing to cellular damage through oxidative stress and apoptotic mechanisms mediated by the Reaper and DIAP1 proteins. Additionally, the composition analysis of vape liquid revealed the presence of propylene glycol, nicotine, methyl esters, and an unidentified compound. This study highlights the complex interplay between nicotine, gene expression, and physiological responses in Drosophila.
