Search

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. [ABSTRACT FROM AUTHOR]

Ethnobotanical claims regarding Kigelia africana reported antiulcer properties as part of its medicinal application. In this work, aqueous leaf extract from K. africana was investigated for its phytochemical constituents and antiulcer potential against ethanol-induced ulcer in rats. The participation of oxidative stress on ethanol-induced ulcer and the potential protective antioxidant activity of K. africana extracts were investigated by determining vitamin C and thiobarbituric acid reactive species (TBARS) contents in the gastric mucosa of rats. The HPLC analysis showed the presence of gallic acid, chlorogenic acid, caffeic acid and also the flavonoids rutin, quercetin and kaempferol in the aqueous plant extract. Oral treatment with K. africana extract (1.75; 3.5; 7 and 14 mg/kg) one hour after ulcer induction with ethanol decreased in a dose dependent manner the ulcer index. Ethanol increased significantly stomachal TBARS levels and decreased vitamin C content when compared to the control animals. K. africana blunted the ethanol-induced oxidative stress and restored vitamin C content to the control levels. The present results indicate that the aqueous leaf extract from K. africana possesses antiulcer potential. The presence of flavonoids in plant extract suggests that its antiulcerogenic potential is associated with antioxidant activity. Of particular therapeutic potential, K. africana was effective against ethanol even after the induction of ulcer, indicating that it can have protective and curative effects against gastric lesion.