Impact of nicotine exposure on hair cell toxicity and embryotoxicity during Zebrafish development

Myung Hoon Yoo, Yoon Chan Rah, Saemi Park, Soonil Koun, Gi Jung Im, Sungwon Chae, Hak Hyun Jung, June Choi

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)109-117
Number of pages9
JournalClinical and Experimental Otorhinolaryngology
Volume11
Issue number2
DOIs
Publication statusPublished - 2018 Jun 1

Fingerprint

Zebrafish
Nicotine
In Situ Nick-End Labeling
Mortality
Embryonic Structures
Heart Rate
Apoptosis
Maternal Exposure
DNA Nucleotidylexotransferase
Iodides
Biotin
Electron Scanning Microscopy
Ear
Control Groups

Keywords

  • Embryotoxicity
  • Hair cells
  • Nicotine
  • Ototoxicity
  • Tobacco
  • Zebrafish

ASJC Scopus subject areas

  • Surgery
  • Otorhinolaryngology

Cite this

Impact of nicotine exposure on hair cell toxicity and embryotoxicity during Zebrafish development. / Yoo, Myung Hoon; Rah, Yoon Chan; Park, Saemi; Koun, Soonil; Im, Gi Jung; Chae, Sungwon; Jung, Hak Hyun; Choi, June.

In: Clinical and Experimental Otorhinolaryngology, Vol. 11, No. 2, 01.06.2018, p. 109-117.

Research output: Contribution to journalArticle

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title = "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.",
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N2 - 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.

AB - 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.

KW - Embryotoxicity

KW - Hair cells

KW - Nicotine

KW - Ototoxicity

KW - Tobacco

KW - Zebrafish

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