Abstract
Age-related hearing loss (ARHL) is an increasing and gradual sensorineural hearing dysfunction. Oxidative stress is an essential factor in developing ARHL; additionally, premature senescence of auditory cells induced by oxidative stress can produce hearing loss. Hydrogen peroxide (H2O2) represents a method commonly used to generate cellular senescence in vitro. The objective of the present paper is to study H2O2-induced senescence patterns in three auditory cell lines (House Ear Institute-Organ of Corti 1, HEI-OC1; organ of Corti, OC-k3, and stria vascularis, SV-k1 cells) to elucidate the intrinsic mechanisms responsible for ARHL. The auditory cells were exposed to H2O2 at different concentrations and times. The results obtained show different responses of the hearing cells concerning cell growth, β-galactosidase activity, morphological changes, mitochondrial activation, levels of oxidative stress, and other markers of cell damage (Forkhead box O3a, FoxO3a, and 8-oxoguanine, 8-oxoG). Comparison between the responses of these auditory cells to H2O2 is a helpful method to evaluate the molecular mechanisms responsible for these auditory cells’ senescence. Furthermore, this in vitro model could help develop anti-senescent therapeutic strategies for the treatment of AHRL.
Highlights
Age-related hearing loss (ARHL), or presbycusis, is a pathology that affects 33% of the population worldwide [1]
The decrease in cell viability is more pronounced at 72 h (p < 0.05) in cells treated with high concentrations of H2 O2 (Figure 2A)
For the first time, the effect of the H2 O2 treatment method in the acquisition over time of the senescence phenotype in three types of auditory cell populations
Summary
Age-related hearing loss (ARHL), or presbycusis, is a pathology that affects 33% of the population worldwide [1]. ARHL is observed simultaneously in both ears in the high frequency spectrum and is a multi-factorial process involving complex interactions between intrinsic (genetic) and extrinsic (environmental) factors [1,2]. ARHL is characterized by cochlear dysfunction, which includes loss of sensory cells, atrophy of the stria vascularis, and loss of the spiral ganglion neurons [1,2]. The mechanisms that have been described are: imbalance between the production of radical oxygen species (ROS) and antioxidants, cumulative mitochondrial dysfunction, accumulation of mitochondrial DNA damage, excitotoxicity, and cellular senescence leading to apoptotic and necrotic auditory cell death [3,4]. The exact biological mechanism of ARHL is still unknown
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