Delayed mitochondrial dysfunction in apoptotic hair cells in chinchilla cochleae following exposure to impulse noise |
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Authors: | Bo Hua Hu |
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Institution: | (1) Center for Hearing and Deafness, State University of New York at Buffalo, 137 Cary Hall, 3435 Main Street, Buffalo, NY 14214, USA |
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Abstract: | Apoptotic death of hair cells (HCs) in the cochlea has been found following exposure to intense noise. The current study was
designed to examine the mitochondrial energetic function of HCs during the course of noise-induced apoptosis. Two aspects
of the mitochondrial energetic function, succinate dehydrogenase (SDH) activity and mitochondrial membrane potential (MMP),
were examined in HCs of chinchilla cochleae following exposure to a series of 75 pairs of impulse noises at 155 dB pSPL. The
results showed that nuclear condensation and uptake of propidium iodide or trypan blue appeared at 10 min after the noise
exposure, indicating a rapid progression of HC apoptosis. However, SDH activity was preserved at this time point. As the time
elapsed (1 hr or 24 hrs) after the noise exposure, all newly-generated apoptotic HCs showed strong SDH activity, indicating
the preservation of SDH activity during the course of apoptosis. Examination of MMP with rhodamine 123 staining revealed that
MMP was sustained in the apoptotic HCs having mild nuclear condensation, even after the occurrence of cell membrane leakage.
MMP was reduced with further progression of nuclear condensation. These results suggest the presence of a delayed mitochondrial
dysfunction in apoptotic HCs following exposure to intense noise.
Research was supported by the Grant NIDCD 1R03 DC006181-01A1. |
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Keywords: | Apoptosis Noise Mitochondrion Chinchilla Mitochondrial membrane potential Succinate dehydrogenase |
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