Nicotine induces mitochondrial fission through mitofusin degradation in human multipotent embryonic carcinoma cells

Biochemical and Biophysical Research Communications
Naoya HirataYasunari Kanda

Abstract

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 c...Continue Reading

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Citations

Jun 16, 2018·Nanotoxicology·Shigeru YamadaYasunari Kanda
Dec 7, 2018·The Journal of Toxicological Sciences·Shigeru YamadaYasunari Kanda
Jun 15, 2019·Journal of Bioenergetics and Biomembranes·Dominika MalińskaJoanna Szczepanowska
Jul 11, 2020·Cells·Ana Paula Magalhães RebeloMarta Giacomello
Mar 7, 2021·Biomedicines·Nuno Santos Leal, Luís Miguel Martins

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