Cellular mechanisms of noise-induced hearing loss

Abstract

Exposure to intense sound or noise can result in purely temporary threshold shift (TTS), or leave a residual permanent threshold shift (PTS) along with alterations in growth functions of auditory nerve output. Recent research has revealed a number of mechanisms that contribute to noise-induced hearing loss (NIHL). The principle cause of NIHL is damage to cochlear hair cells and associated synaptopathy. Contributions to TTS include reversible damage to hair cell (HC) stereocilia or synapses, while moderate TTS reflects protective purinergic hearing adaptation. PTS represents permanent damage to or loss of HCs and synapses. While the substrates of HC damage are complex, they include the accumulation of reactive oxygen species and the active stimulation of intracellular stress pathways, leading to programmed and/or necrotic cell death. Permanent damage to cochlear neurons can also contribute to the effects of NIHL, in addition to HC damage. These mechanisms have translational potential for pharmacological intervention and provide multiple opportunities to prevent HC damage or to rescue HCs and spiral ganglion neurons that have suffered injury. This paper reviews advances in our understanding of cellular mechanisms that contribute to NIHL and their potential for therapeutic manipulation.

2,3,4′,5-Tetrahydroxystilbene-2-O-β-D-Glucoside (THSG) Activates the Nrf2 Antioxidant Pathway and Attenuates Oxidative Stress-Induced Cell Death in Mouse Cochlear UB/OC-2 Cells

“…Hearing loss is a serious global morbidity that affects 360 million people worldwide [1], and this neurological disability impacts both the physical and mental health of patients [2]. Recent research has revealed several mechanisms and molecules that contribute to hearing loss, such as oxidative stress and apoptotic cell death [3]. Oxidative stress plays a critical role in the pathogenesis of hearing loss and in diabetes-related and environmental/occupational exposure-associated complications [4,5].…”

“…The available evidence suggests that excessive oxidative stress in the cochlea is closely related to the pathogenesis of hearing loss [3,6]. Therefore, pharmacologically reducing oxidative stress and strengthening the cochlear resistance against oxidative stress and cytotoxic chemicals are effective prevention strategies for maintaining the structural and functional integrity of the cochlea to prevent the development and progression of hearing loss.…”

Frequency of Noise Induced Hearing Loss Among Traffic Wardens of Lahore

“…10 The mechanism of damage includes accretion of the reactive oxygen genus and stimulation of the intracellular stress pathway, that leads to cell death. 11 Hearing loss due to cochlear dysfunction also changes the organization of the central auditory pathway. 12 Varying degrees of permanent deafness occurs due to damage to inner ear.…”

Cortical pattern of reduced perfusion in hearing loss revealed by ASL‐MRI

“…Finally, from the metabolic perspective, using 18 F‐fluro‐deoxy‐glucose (FDG) positron Emission Tomography (PET), Verger et al () have revealed a specific pattern of decreased regional cerebral blood flow (CBF), a quantitative measure of baseline neuronal metabolism, in the associative auditory cortex of HL patients (mainly in the right hemisphere). While HL is frequently caused by accumulated noise and ototoxic experiences that produce a loss of sensory cells in the cochlea (Kurabi, Keithley, Housley, Ryan, & Wong, ), a possible reduction in the regional CBF in the auditory cortex may also indicate the presence of a vascular dysfunction, which could lead itself to neuronal deficits. In fact, because CBF is regulated according to local neuronal activity and metabolism (i.e., neurovascular coupling; Iadecola, ), if CBF deficiency is prior to neurodegeneration, a reduced CBF in the central auditory system of HL patients could be linked to a reduced dilatory capacity of cerebral vasculature in upregulating perfusion, with an increased risk for vascular disease and a higher vulnerability for neurological disorders in aging (Gao et al, ).…”