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|dc.title||L-N-Acetylcysteine protects against radiation-induced apoptosis in a cochlear cell line|
|dc.identifier.citation||Low, W.-K., Sun, L., Tan, M.G.K., Chua, A.W.C., Wang, D.-Y. (2008). L-N-Acetylcysteine protects against radiation-induced apoptosis in a cochlear cell line. Acta Oto-Laryngologica 128 (4) : 440-445. ScholarBank@NUS Repository. https://doi.org/10.1080/00016480701762490|
|dc.description.abstract||Conclusion. L-N-Acetylcysteine (L-NAC) significantly reduced reactive oxygen species (ROS) generation and cochlear cell apoptosis after irradiation. The safe and effective use of L-NAC in reducing radiation-induced sensorineural hearing loss (SNHL) should be verified by further in vivo studies. Objectives. Radiation-induced SNHL is a common complication after radiotherapy of head and neck tumours. There is growing evidence to suggest that ROS play an important role in apoptotic cochlear cell death from ototoxicity, resulting in SNHL. The aim of this study was to evaluate the effectiveness of L-NAC, an antioxidant, on radiation-induced apoptosis in cochlear cells. Materials and methods. The OC-k3 cochlear cell line was studied after 0 and 20 Gy of γ-irradiation. Cell viability assay was performed using 3-[4,5-dimethylthiazol-2-yl]-2,5- diphenyltetrazolium bromide. Flow cytometry and TUNEL assay were done with and without the addition of 10 mmol/L of L-NAC. Intracellular generation of ROS was detected by 2′,7′-dichlorofluorescein diacetate, with comparisons made using fluorescence intensity. Results. L-NAC increased the viability of cells after irradiation. Generation of ROS was demonstrated at 1 h post-irradiation and was significantly reduced by L-NAC (p|
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