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Acta Otolaryngol. 2010 Jun;130(6):670-8. doi: 10.3109/00016480903428200.

Gentamicin-induced spiral ganglion cell death: apoptosis mediated by ROS and the JNK signaling pathway.

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Department of Otolaryngology-Head and Neck Surgery, College of Medicine, Dong-A University, Busan, Korea.



Reactive oxygen species (ROS) and the c-Jun N-terminal kinase (JNK) signaling pathway may be involved in secondary apoptosis of spiral ganglion cells (SGCs) induced by intracochlear gentamicin injection.


The purpose of this study was to ascertain the role of ROS and the JNK signaling pathway in secondary apoptosis of SGCs induced by intracochlear gentamicin treatment.


Gentamicin (40 mg/ml) was injected into the cochlea of guinea pigs (n = 18) to destroy the hair cells and induce secondary apoptosis of SGCs. At 1 (n = 6), 2 (n = 6), and 3 (n = 6) weeks after gentamicin treatment, the cochleas were removed and stained with hematoxylin and eosin, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling to observe the morphologic changes and apoptosis of SGCs. A dihydroethidium (DHE) assay was performed to detect ROS generation, and RT-PCR and Western blot analysis were used to assess the expression of Fas ligand (FasL), JNK, and c-Jun.


After gentamicin was injected into the cochlea, apoptosis and progressive loss of SGCs were observed. RT-PCR and Western blot analysis showed increased expression of FasL after gentamicin treatment. ROS generation detected by DHE fluorescence increased progressively, and the expression of JNK, phospho-JNK, c-Jun, and phospho-c-Jun also increased.

[Indexed for MEDLINE]

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