Impact of Nicotine Exposure on Hair Cell Toxicity and Embryotoxicity During Zebrafish Development

Abstract

Objectives Nicotine has various adverse effects including negative impacts associated with maternal exposure. In the current study, we examined nicotine-induced damage of hair cells and embryotoxicity during zebrafish development.Methods Zebrafish embryos were exposed to nicotine at several concentrations (5, 10, 20, and 40 μM) and embryotoxicity were evaluated at 72 hours, including hatching rate, mortality, teratogenicity rate, and heart rate. Hair cells within the supraorbital (SO1 and SO2), otic (O1), and occipital (OC1) neuromasts were identified at 120 hours. Apoptosis and mitochondrial damage of hair cells were analyzed using TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling) and DASPEI (2-[4-(dimethylamino)styryl]-N-ethylpyridinium iodide) assays, respectively, and changes of ultrastructure were observed by scanning electron microscopy.Results The control group without nicotine appeared normal with overall mortality and teratogenicity rate <5%. The hatching rate and mortality rate was not significantly different according to nicotine concentration (n=400 each). The abnormal morphology rate (n=400) increased and heart rate (n=150) decreased with increasing nicotine concentration (P<0.05). Nicotine-induced hair cell damage significantly increased as nicotine concentration increased. A significantly greater number of TUNEL-positive cells (P<0.01) and markedly smaller DASPEI area (P<0.01) were shown as nicotine concentration increased.Conclusion The current results suggest that nicotine induces dose-dependent hair cell toxicity in embryos by promoting apoptosis and mitochondrial and structural damage.

In vivo assessment of the toxicity of electronic cigarettes to zebrafish (Danio rerio) embryos, following gestational exposure, in terms of mortality, developmental toxicity, and hair cell damage: Toxicity of E-cigs to zebrafish embryos

“…The average number of hair cells in two main regions, the anterior lateral line (ALL) system, including the supraorbital [SO1 and SO2], otic [O1], and occipital [OC1] nerves, and the posterior lateral line (PLL) system, including the neuromasts of the trunk and tail of zebrafishes (p 3–6), was determined using a fluorescence microscope at 7 dpf (LSM5 PASCAL; Carl Zeiss, Germany). 9,17,18,25,27 The hair cells were identified by our two experts, and they were evaluated in all experimental and control conditions (n = 29–40 for each of the concentrations)…”

“…The toxic effect of E-cig usage during pregnancy has been also addressed; the results demonstrated that the nicotine consumed during the use of E-cigs is similar to that consumed during conventional cigarette smoking. 8 Numerous animal studies have confirmed the toxic effects of nicotine to the developing fetus; 9,10 the effects of nicotine exposure by E-cig usage during fetal development is suggested to be similar to those by conventional cigarette smoking. 8,11 However, the constituents and potential adverse effects of E-cigs are not well understood; 3,11,12 moreover, there is a dearth of scientific information pertaining to the hazards of these substances to gestational development and sensory hair cells.…”

The importance of pH: How aquarium water is affecting behavioural responses to drug exposure in larval zebrafish

“…To study the effect of pH on different drug conditions, four commonly used drugs of abuse were selected for this study. Nicotine (Sigma-Aldrich) was administered at a concentration of 5 µM (García-González et al, 2020;Petzold et al, 2009;Yoo et al, 2018), morphine sulphate (Sigma-Aldrich) was administered at 2.6 µM (Lopez-Luna et al, 2017), d-amphetamine (Sigma-Aldrich) was administered at 22 µM (Irons et al, 2010), and caffeine (Tocris) was administered at 200 µM (Gutiérrez et al, 2020). Concentrations were based on a combination of larval and adult zebrafish studies investigating effects on locomotor activity.…”

Resveratrol Protects Against Nicotine-Induced Apoptosis by Enhancing Autophagy in BEAS-2B Lung Epithelial Cells

“…4 Research has shown that upon cell entry through nicotinic acetylcholine receptors (nAChRs), Nic can induce apoptosis in a variety of cell types, including lung epithelial cells. 5,6 Although lung epithelial cells are not classic phagocytes, they are the first line of defense against invading microorganisms and are involved in bacterial uptake and clearance. 7,8 Moreover, a role for lung epithelial cell apoptosis has been demonstrated in the development and progression of COPD.…”