In vitro effects of hydrogen peroxide on the cochlear neurosensory epithelium of the guinea pig

• Published in: Hearing research 2000-05, Vol.143 (1), p.162-170
• Main Authors: Dehne, N., Lautermann, J., ten Cate, W.-J.F., Rauen, U., de Groot, H.
• Format: Article
• Language: English
• Subjects: 2,2'-Dipyridyl - pharmacology; Aminoquinolines - pharmacology; Animals; Antioxidant; Biological and medical sciences; Calcium; Calcium Channel Blockers - pharmacology; Cell Survival - drug effects; Chelating Agents - pharmacology; Cochlea - cytology; Cochlea - drug effects; Cochlea - physiology; Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation; Epithelial Cells - drug effects; Epithelial Cells - physiology; Fundamental and applied biological sciences. Psychology; Guinea Pigs; Hair Cells, Auditory, Inner - drug effects; Hair Cells, Auditory, Inner - physiology; Hair Cells, Auditory, Outer - drug effects; Hair Cells, Auditory, Outer - physiology; Hydrogen Peroxide - pharmacology; In Vitro Techniques; Iron; Neuroprotective Agents - pharmacology; Nifedipine - pharmacology; Organ of Corti; Reactive oxygen species; Time Factors; Vertebrates: nervous system and sense organs
• ISSN: 0378-5955; 1878-5891
• DOI: 10.1016/S0378-5955(00)00036-8

Reactive oxygen species (ROS) have been postulated to be involved in drug ototoxicity and noise-induced hearing loss. Hydrogen peroxide (H 2O 2)-induced cell damage in the inner ear was investigated using the neurosensory epithelium of a guinea pig cochlea. Hair cells and supporting cells of the epithelium incubated in Hanks’ balanced salt solution were viable up to 6 h. After 2 h of treatment with 0.2 mM H 2O 2 about 85% of the outer hair cells lost their viability. In contrast inner hair cells slowly began to die after 2 h of H 2O 2 treatment. The Deiters cells and Hensen cells did not show any signs of damage in the presence of H 2O 2. Nifedipine, a calcium channel blocker, Quin-2 AM, an intracellular calcium chelator, and 2,2′-dipyridyl, a membrane-permeable iron chelator, all provided partial protection against H 2O 2-induced outer hair cell death. The combination of both chelators showed an additional protective effect. The antioxidants N-acetylcysteine and glutathione-monoethyl ester completely protected against H 2O 2 damage. These results suggest that calcium, iron, and thiol homeostasis play a crucial role in hair cell death caused by H 2O 2.