Selective Vulnerability of the Cochlear Basal Turn to Acrylonitrile and Noise

Abstract

Exposure to acrylonitrile, a high-production industrial chemical, can promote noise-induced hearing loss (NIHL) in the rat even though this agent does not itself produce permanent hearing loss. The mechanism by which acrylonitrile promotes NIHL includes oxidative stress as antioxidant drugs can partially protect the cochlea from acrylonitrile + noise. Acrylonitrile depletes glutathione levels while noise can increase the formation of reactive oxygen species. It was previously noted that the high-frequency or basal turn of the cochlea was particularly vulnerable to the combined effects of acrylonitrile and noise when the octave band noise (OBN) was centered at 8 kHz. Normally, such a noise would be expected to yield damage at a more apical region of the cochlea. The present study was designed to determine whether the basal cochlea is selectively sensitive to acrylonitrile or whether, by adjusting the frequency of the noise band, it would be possible to control the region of the auditory impairment. Rats were exposed to one of three different OBNs centered at different frequencies (4 kHz, 110 dB and 8 or 16 kHz at 97 dB) for 5 days, with and without administration of acrylonitrile (50 mg/kg/day). The noise was set to cause limited NIHL by itself. Auditory function was monitored by recording distortion products, by compound action potentials, and by performing cochlear histology. While the ACN-only and noise-only exposures induced no or little permanent auditory loss, the three exposures to acrylonitrile + noise produced similar auditory and cochlear impairments above 16 kHz, despite the fact that the noise exposures covered 2 octaves. These observations show that the basal cochlea is much more sensitive to acrylonitrile + noise than the apical partition. They provide an initial basis for distinguishing the pattern of cochlear injury that results from noise exposure from that which occurs due to the combined effects of noise and a chemical contaminant.

Metalloproteinases and Their Associated Genes Contribute to the Functional Integrity and Noise-Induced Damage in the Cochlear Sensory Epithelium

“…The apical and basal regions of the cochlear sensory epithelium are known to have different susceptibilities to acoustic trauma (Thorne et al, 1984; Bohne et al, 1987; Hu et al, 2002; Pouyatos et al, 2009). We sought to determine whether the expression patterns of MMPs and their related genes differed in these two regions.…”

Activation of the antigen presentation function of mononuclear phagocyte populations associated with the basilar membrane of the cochlea after acoustic overstimulation

“…The functional implications of the apical and basal difference in macrophage properties are not clear. It has been documented in previous studies that the sensory cells in the basal section of the cochlea are more susceptible than the apical sensory cells to pathological insults, including ototoxicity, aging and acoustic injury (Pouyatos et al, 2009; Sha et al, 2001; Yang et al, 2013). The immune difference may contribute to this site-specific vulnerability.…”

Transcriptional changes in adhesion-related genes are site-specific during noise-induced cochlear pathogenesis

“…Functionally, the basal end exhibits less antioxidant capacity, and is prone to oxidative stress (Sha et al, 2001), while basal sensory cells exhibit a higher susceptibility to ototoxicity and age-related degeneration (Fechter et al, 1997; Forge and Schacht, 2000; Sha et al, 2001). Importantly, previous investigations have demonstrated a greater vulnerability to acoustic injury in the basal sensory cells (Bohne et al, 1987; Hu et al, 2002b; Pouyatos et al, 2009; Thorne et al, 1984). These spatial differences in the properties of the sensory epithelium prompted us to investigate site-specific changes in the expression levels of adhesion-related genes.…”