Abstract
Excessive superoxide radical production by mitochondria is one of the underlying causes of noise‐induced damage to tissues in the inner ear. Mitochondria are highly dynamic organelles that are maintained by the opposing processes of fusion and fission, events which alter mitochondrial morphology, biogenesis, and energy metabolism. The HEI‐OC1 auditory cell line possesses a highly interconnected mitochondrial network structure under normal growth conditions as revealed by immunolabeling for Tom20. Treatment with antimycin A increased fission processes resulting in a primary population of punctate and donut‐shaped mitochondria. Inhibition of dynamin related protein 1 effectively reduced mitochondrial fission and reactive oxygen species production and increased cell survival following antimycin A treatment. Super‐resolution imaging of Tom20 immunolabeled mitochondria in murine inner ear cells showed primarily punctate mitochondria in auditory outer hair cells, a mixed population of punctate and intermediate length mitochondria in inner hair cells, and elongated mitochondria in Deiters' cells. These results indicate that even under ambient noise conditions, it is likely that outer hair cells place high energy demands on their mitochondria. The punctate mitochondrial morphology in this cell type suggests that the balance of fission and fusion processes is altered, potentially due to a higher oxidant environment being present in these cells.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have