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Oxidative damage to mitochondrial DNA (mtDNA) and cell apoptosis are heavily implicated in aging. Our previous study established a mimetic rat model of aging in the cochleae using D‑galactose (D‑gal), and revealed that chronic injection of D‑gal can increase oxidative stress and mtDNA common deletions (CD). The aim of the present study was to investigate the sources of reactive oxygen species and the occurrence of apoptosis in the cochleae of rats following 8 weeks of D‑gal exposure. The results of the present study indicated that an elevated accumulation of the mtDNA CD and mitochondrial ultrastructural damage occurred in the cochleae of rats injected with D‑gal for 8 weeks. In addition, the levels of 8‑hydroxy‑2‑deoxyguanosine, NADPH oxidase (NOX) 3, P22phox and cleaved caspase 3, and the number of terminal deoxynucleotidyl transferase‑mediated deoxyuridine triphosphate nick‑end‑labelling‑positive cells were increased in the cochleae of D‑gal‑treated rats, compared with the controls. These findings suggested that nitric oxide synthase NOX3‑associated oxidative stress may contribute to the accumulation of mtDNA mutations and activate a caspase 3‑dependent apoptotic signalling pathway in the cochleae during aging. The present study also provided novel insights into the development of age‑associated hearing loss, also termed presbycusis.

NADPH oxidase 3-associated oxidative stress and caspase 3-dependent apoptosis in the cochleae of D-galactose-induced aged rats