Protective role of NecroX-5 against neomycin-induced hair cell damage in zebrafish

June Choi; Jae-Jun Song; Jiwon Chang; Jungim Choi; Gi Jung Im; Sungwon Chae; Seung Hoon Lee; Soon Young Kwon; Hak Hyun Jung; Ah Young Chung; Hae Chul Park

doi:10.1007/s00204-013-1124-3

Protective role of NecroX-5 against neomycin-induced hair cell damage in zebrafish

June Choi, Jae-Jun Song, Jiwon Chang, Jungim Choi, Gi Jung Im, Sungwon Chae, Seung Hoon Lee, Soon Young Kwon, Hak Hyun Jung, Ah Young Chung, Hae Chul Park

Department of Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

15 Citations (Scopus)

Abstract

NecroX-5, one of the derivatives of NecroX series compounds, is a mitochondrial reactive oxygen species and reactive nitrogen species scavenger that inhibits cell death against various kinds of oxidative stresses. The objective of the present study was to evaluate the effects of NecroX-5 on neomycin-induced ototoxicity in transgenic zebrafish (Brn3C: EGFP). Five days post-fertilization, zebrafish larvae were exposed to 125 μM neomycin and one of the following NecroX-5 concentrations for 1 h: 10, 25, 50, and 75 μM. Hair cells within the neuromasts of the supraorbital (SO1 and SO2), otic (O1), and occipital (OC1) lateral lines were analyzed using fluorescence microscopy (n = 10). The terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay and 2-[4-(dimethylamino) styryl]-N-ethylpyridiniumiodide (DASPEI) assay were performed for evaluation of apoptosis and mitochondrial damage. Ultrastructural changes were evaluated using scanning electron microscopy. NecroX-5 decreased neomycin-induced hair cell loss in the neuromasts (NecroX-5 50 μM: 13.4 ± 2.0 cells, 125 μM neomycin only: 8.1 ± 1.2 cells; n = 10, P < 0.05) and decreased the TUNEL reaction. The ultrastructural analysis showed that the structures of mitochondria and hair cells within the neuromasts were preserved in zebrafish exposed to 125 μM neomycin and 50 μM NecroX-5. NecroX-5 decreased apoptosis and mitochondrial damage. In conclusion, NecroX-5 attenuated neomycin-induced hair cell loss in zebrafish.

Original language	English
Pages (from-to)	435-441
Number of pages	7
Journal	Archives of Toxicology
Volume	88
Issue number	2
DOIs	https://doi.org/10.1007/s00204-013-1124-3
Publication status	Published - 2014 Feb

Keywords

NecroX-5
Neomycin
Ototoxicity
Zebrafish

ASJC Scopus subject areas

Toxicology
Health, Toxicology and Mutagenesis

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10.1007/s00204-013-1124-3

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@article{0341ce5ed20f4497bb7d3e4f5ffb3f24,

title = "Protective role of NecroX-5 against neomycin-induced hair cell damage in zebrafish",

abstract = "NecroX-5, one of the derivatives of NecroX series compounds, is a mitochondrial reactive oxygen species and reactive nitrogen species scavenger that inhibits cell death against various kinds of oxidative stresses. The objective of the present study was to evaluate the effects of NecroX-5 on neomycin-induced ototoxicity in transgenic zebrafish (Brn3C: EGFP). Five days post-fertilization, zebrafish larvae were exposed to 125 μM neomycin and one of the following NecroX-5 concentrations for 1 h: 10, 25, 50, and 75 μM. Hair cells within the neuromasts of the supraorbital (SO1 and SO2), otic (O1), and occipital (OC1) lateral lines were analyzed using fluorescence microscopy (n = 10). The terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay and 2-[4-(dimethylamino) styryl]-N-ethylpyridiniumiodide (DASPEI) assay were performed for evaluation of apoptosis and mitochondrial damage. Ultrastructural changes were evaluated using scanning electron microscopy. NecroX-5 decreased neomycin-induced hair cell loss in the neuromasts (NecroX-5 50 μM: 13.4 ± 2.0 cells, 125 μM neomycin only: 8.1 ± 1.2 cells; n = 10, P < 0.05) and decreased the TUNEL reaction. The ultrastructural analysis showed that the structures of mitochondria and hair cells within the neuromasts were preserved in zebrafish exposed to 125 μM neomycin and 50 μM NecroX-5. NecroX-5 decreased apoptosis and mitochondrial damage. In conclusion, NecroX-5 attenuated neomycin-induced hair cell loss in zebrafish.",

keywords = "NecroX-5, Neomycin, Ototoxicity, Zebrafish",

author = "June Choi and Jae-Jun Song and Jiwon Chang and Jungim Choi and Im, {Gi Jung} and Sungwon Chae and Lee, {Seung Hoon} and Kwon, {Soon Young} and Jung, {Hak Hyun} and Chung, {Ah Young} and Park, {Hae Chul}",

note = "Funding Information: Acknowledgments This research was supported by a Korea University Grant, by the Soo ENT Clinic and the Communication Disorders Center, Korea University, and by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2010-0006038).",

year = "2014",

month = feb,

doi = "10.1007/s00204-013-1124-3",

language = "English",

volume = "88",

pages = "435--441",

journal = "Archives of Toxicology",

issn = "0340-5761",

publisher = "Springer Verlag",

number = "2",

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TY - JOUR

T1 - Protective role of NecroX-5 against neomycin-induced hair cell damage in zebrafish

AU - Choi, June

AU - Song, Jae-Jun

AU - Chang, Jiwon

AU - Choi, Jungim

AU - Im, Gi Jung

AU - Chae, Sungwon

AU - Lee, Seung Hoon

AU - Kwon, Soon Young

AU - Jung, Hak Hyun

AU - Chung, Ah Young

AU - Park, Hae Chul

N1 - Funding Information: Acknowledgments This research was supported by a Korea University Grant, by the Soo ENT Clinic and the Communication Disorders Center, Korea University, and by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2010-0006038).

PY - 2014/2

Y1 - 2014/2

N2 - NecroX-5, one of the derivatives of NecroX series compounds, is a mitochondrial reactive oxygen species and reactive nitrogen species scavenger that inhibits cell death against various kinds of oxidative stresses. The objective of the present study was to evaluate the effects of NecroX-5 on neomycin-induced ototoxicity in transgenic zebrafish (Brn3C: EGFP). Five days post-fertilization, zebrafish larvae were exposed to 125 μM neomycin and one of the following NecroX-5 concentrations for 1 h: 10, 25, 50, and 75 μM. Hair cells within the neuromasts of the supraorbital (SO1 and SO2), otic (O1), and occipital (OC1) lateral lines were analyzed using fluorescence microscopy (n = 10). The terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay and 2-[4-(dimethylamino) styryl]-N-ethylpyridiniumiodide (DASPEI) assay were performed for evaluation of apoptosis and mitochondrial damage. Ultrastructural changes were evaluated using scanning electron microscopy. NecroX-5 decreased neomycin-induced hair cell loss in the neuromasts (NecroX-5 50 μM: 13.4 ± 2.0 cells, 125 μM neomycin only: 8.1 ± 1.2 cells; n = 10, P < 0.05) and decreased the TUNEL reaction. The ultrastructural analysis showed that the structures of mitochondria and hair cells within the neuromasts were preserved in zebrafish exposed to 125 μM neomycin and 50 μM NecroX-5. NecroX-5 decreased apoptosis and mitochondrial damage. In conclusion, NecroX-5 attenuated neomycin-induced hair cell loss in zebrafish.

AB - NecroX-5, one of the derivatives of NecroX series compounds, is a mitochondrial reactive oxygen species and reactive nitrogen species scavenger that inhibits cell death against various kinds of oxidative stresses. The objective of the present study was to evaluate the effects of NecroX-5 on neomycin-induced ototoxicity in transgenic zebrafish (Brn3C: EGFP). Five days post-fertilization, zebrafish larvae were exposed to 125 μM neomycin and one of the following NecroX-5 concentrations for 1 h: 10, 25, 50, and 75 μM. Hair cells within the neuromasts of the supraorbital (SO1 and SO2), otic (O1), and occipital (OC1) lateral lines were analyzed using fluorescence microscopy (n = 10). The terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay and 2-[4-(dimethylamino) styryl]-N-ethylpyridiniumiodide (DASPEI) assay were performed for evaluation of apoptosis and mitochondrial damage. Ultrastructural changes were evaluated using scanning electron microscopy. NecroX-5 decreased neomycin-induced hair cell loss in the neuromasts (NecroX-5 50 μM: 13.4 ± 2.0 cells, 125 μM neomycin only: 8.1 ± 1.2 cells; n = 10, P < 0.05) and decreased the TUNEL reaction. The ultrastructural analysis showed that the structures of mitochondria and hair cells within the neuromasts were preserved in zebrafish exposed to 125 μM neomycin and 50 μM NecroX-5. NecroX-5 decreased apoptosis and mitochondrial damage. In conclusion, NecroX-5 attenuated neomycin-induced hair cell loss in zebrafish.

KW - NecroX-5

KW - Neomycin

KW - Ototoxicity

KW - Zebrafish

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U2 - 10.1007/s00204-013-1124-3

DO - 10.1007/s00204-013-1124-3

M3 - Article

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AN - SCOPUS:84893976835

SN - 0340-5761

VL - 88

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EP - 441

JO - Archives of Toxicology

JF - Archives of Toxicology

IS - 2

ER -

Protective role of NecroX-5 against neomycin-induced hair cell damage in zebrafish

Abstract

Keywords

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