Abstract
Noise exposure is the most important external factor causing acquired hearing loss in humans, and it is strongly associated with the production of reactive oxygen species (ROS) in the cochlea. Several studies reported that the administration of various compounds with antioxidant effects can treat oxidative stress-induced hearing loss. However, traditional systemic drug administration to the human inner ear is problematic and has not been successful in a clinical setting. Thus, there is an urgent need to develop rescue treatment for patients with acute acoustic injuries. Hydrogen gas has antioxidant effects, rapid distribution, and distributes systemically after inhalation.The purpose of this study was to determine the protective efficacy of a single dose of molecular hydrogen (H2) on cochlear structures. Guinea pigs were divided into six groups and sacrificed immediately after or at 1 or 2 weeks. The animals were exposed to broadband noise for 2 h directly followed by 1-h inhalation of 2% H2 or room air. Electrophysiological hearing thresholds using frequency-specific auditory brainstem response (ABR) were measured prior to noise exposure and before sacrifice. ABR thresholds were significantly lower in H2-treated animals at 2 weeks after exposure, with significant preservation of outer hair cells in the entire cochlea. Quantification of synaptophysin immunoreactivity revealed that H2 inhalation protected the cochlear inner hair cell synaptic structures containing synaptophysin. The inflammatory response was greater in the stria vascularis, showing increased Iba1 due to H2 inhalation.Repeated administration of H2 inhalation may further improve the therapeutic effect. This animal model does not reproduce conditions in humans, highlighting the need for additional real-life studies in humans.
Highlights
Worldwide, there is growing interest in pharmacological treatments to protect the inner ear during harmful exposure and treat inner ear disorders
There may be a prolonged overexpression of reactive oxygen species (ROS) in cochlear tissue after acoustic overstimulation that persists for 2 weeks (Mattson, 2000; Yamashita et al, 2004; Henderson et al, 2006)
Immune reactions follow acoustic overstimulation which can initially be seen as the release of proinflammatory cytokines and stimulation of innate receptors found in the macrophages/microglia (Wakabayashi et al, 2010; Vethanayagam et al, 2016)
Summary
There is growing interest in pharmacological treatments to protect the inner ear during harmful exposure and treat inner ear disorders. Noise-induced hearing loss (NIHL) results from oxidative stress, mitochondrial damage, and excessive glutamate release at the synapse between the IHC and its afferent neuron, the inner hair cell ribbon synapse (Pujol and Puel, 1999; Hu et al, 2002). Elevated formation of ROS and free radicals is considered an important factor in producing OHC loss and is seen as a key factor for pharmacological prevention and treatment of NIHL (Yamashita et al, 2004; Rybak et al, 2019). ROS are overproduced during intense noise in various cochlear cells, including OHCs, blood vessel cells, supporting cells, and spiral ganglion neurons (Mattson, 2000; Yamashita et al, 2004; Henderson et al, 2006). The inflammatory process involves recruiting immune cells of both the innate and adaptive systems (Hirose et al, 2005; Wakabayashi et al, 2010; Wood and Zuo, 2017)
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