Oxidative stress and inflammation in age-related hearing loss: temporal dynamics in cochlear degeneration of C57BL/6 mice.

Abstract

BACKGROUND: Age-related hearing loss (ARHL) is a condition linked to cochlear degeneration influenced by genetic, environmental, and comorbid factors. Although oxidative stress and inflammation have been implicated in ARHL, their dynamic interplay during aging remains unclear. AIMS/OBJECTIVES: This study aimed to clarify the temporal progression of oxidative and inflammatory mechanisms in cochlear degeneration using the C57BL/6 mouse model of ARHL. MATERIAL AND METHODS: C57BL/6 mice, characterized by a predictable auditory decline, were examined at 3, 6, and 12 months of age. Auditory brainstem responses (ABRs) were recorded to assess hearing thresholds and neural transmission efficiency. Morphological analyses were performed to evaluate neuronal integrity, while cochlear tissues were analyzed for markers of oxidative stress and inflammation, including 3-nitrotyrosine (3-NT), 4-hydroxynonenal (4-HNE), and tumor necrosis factor-alpha (TNF-α). RESULTS: With advancing age, mice exhibited a progressive elevation of hearing thresholds, reduced neural transmission efficiency, and loss of spiral ganglion neurons. Molecular analyses revealed increased 3-NT, 4-HNE, and TNF-α expression. Both oxidative stress and inflammation were detectable from 6 months of age, suggesting that these processes synergistically drive cochlear degeneration. CONCLUSIONS AND SIGNIFICANCE: Our findings underscore the role of oxidative stress-inflammation crosstalk in ARHL, suggesting therapeutic targets for preventing presbycusis in aging populations.