The impact of mitochondrial energetic dysfunction on apoptosis in outer hair cells of the cochlea following exposure to intense noise.

Previous studies have shown that exposure to intense noise causes outer hair cells (OHCs) to die, primarily through the process of apoptotic degeneration. The current study was designed to examine the regulatory role of mitochondrial bioenergetic function in controlling the initiation and execution of the apoptotic process of OHCs. Chinchilla cochleae were treated with 3-nitropropionic acid (3-NP, 20 or 50mM), an irreversible inhibitor of succinate dehydrogenase (SDH), to inhibit the mitochondrial energy production before and after exposure to 75 pairs of impulses at 155dB pSPL. Comparison of the noise-exposed cochleae treated with and without 3-NP revealed that the inhibition of SDH activity delayed nuclear degradation in apoptotic OHCs. However, the initiation of apoptosis appeared to be undeterred. There was no major shift of cell death pathways from apoptosis to necrosis, although a small portion of OHCs showed signs of secondary necrosis. Collectively, the results of the study suggest that, while the mitochondrial energetic function plays an important role in regulating the apoptotic process, its dysfunction has a limited influence on the suppression of apoptotic induction in OHCs following exposure to intense noise.