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Nicotine is considered to contribute to the health risks associated with cigarette smoking. Nicotine exerts its cellular functions by acting on nicotinic acetylcholine receptors (nAChRs), and adversely affects normal embryonic development. However, nicotine toxicity has not been elucidated in human embryonic stage. In the present study, we examined the cytotoxic effects of nicotine in human multipotent embryonal carcinoma cell line NT2/D1. We found that exposure to 10 μM nicotine decreased intracellular ATP levels and inhibited proliferation of NT2/D1 cells. Because nicotine suppressed energy production, which is a critical mitochondrial function, we further assessed the effects of nicotine on mitochondrial dynamics. Staining with MitoTracker revealed that 10 μM nicotine induced mitochondrial fragmentation. The levels of the mitochondrial fusion proteins, mitofusins 1 and 2, were also reduced in cells exposed to nicotine. These nicotine effects were blocked by treatment with mecamylamine, a nonselective nAChR antagonist. These data suggest that nicotine degrades mitofusin in NT2/D1 cells and thus induces mitochondrial dysfunction and cell growth inhibition in a nAChR-dependent manner. Thus, mitochondrial function in embryonic cells could be used to assess the developmental toxicity of chemicals.
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http://dx.doi.org/10.1016/j.bbrc.2016.01.063 | DOI Listing |
Toxicol Appl Pharmacol
December 2024
Department of Applied Chemistry and Life Sciences, Graduate School of Engineering, Toyohashi University of Technology, Toyohashi, Aichi 441-8580, Japan; Center for Diversity and Inclusion, Toyohashi University of Technology, Toyohashi, Aichi, 441-8580, Japan. Electronic address:
Concerns have been raised regarding acetamiprid (ACE), a neonicotinoid insecticide, due to its potential neurodevelopmental toxicity. ACE, which is structurally similar to nicotine, acts as an agonist of nicotinic acetylcholine receptors (nAChRs) and resists degradation by acetylcholinesterase. Furthermore, ACE has been reported to disrupt neuronal transmission and induce developmental neurotoxicity and ataxia in animal models.
View Article and Find Full Text PDFLife Sci
December 2024
Department of Anesthesiology, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University & Fujian Emergency Medical Center, Fujian Provincial Key Laboratory of Emergency Medicine, Fujian Provincial Key Laboratory of Critical Medicine, Fujian Provincial Co-constructed Laboratory of "Belt and Road", Fuzhou, Fujian, China. Electronic address:
Aims: Nicotine-exacerbated atherosclerosis significantly increases global mortality. Endothelial cells, which line the interior of blood vessels, are crucial for maintaining vascular function. How nicotine is involved in vascular remodeling in atherosclerosis via modulating endothelial dysfunction remains unknown.
View Article and Find Full Text PDFPharmacol Biochem Behav
December 2024
Swansea Worm Integrative Research Laboratory (SWIRL), Swansea University Medical School, Swansea University, Wales SA2 8PP, United Kingdom.
Nicotine has been shown to induce profound physiological and behavioural responses in invertebrate model organisms such as Caenorhabditis elegans and Drosophila melanogaster. Lumbriculus variegatus is an aquatic oligochaete worm which we have previously demonstrated has application within pharmacological research. Herein, we demonstrate the presence of endogenous acetylcholine and cholinesterase activity within L.
View Article and Find Full Text PDFCancer Prev Res (Phila)
December 2024
University of Chicago Medical Center, United States.
People with HIV (PWH) smoke cigarettes at triple the rate of the general population in the US. Efforts to increase quit rates in this group have met with limited success. The nicotine metabolite ratio (NMR) has shown promise as a phenotypic marker that may be useful in selecting the most appropriate cessation treatments for people who smoke cigarettes.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
January 2025
Environmental Exposures Vascular Disease Institute, Shanxi Medical University, Taiyuan, Shanxi, China.
Pulmonary hypertension is a progressive disease associated with remodeling of the pulmonary vasculature. Excessive proliferation and migration of pulmonary artery smooth muscle cells (PASMCs) play important roles in nicotine-induced vascular injury. Connexin 43 (Cx43) is involved in intracellular communication and regulation of the pulmonary vasculature.
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