Inhalation of molecular hydrogen (2-4%) significantly attenuates ouabain-induced auditory neuropathy in gerbils by reducing apoptosis of spiral ganglion neurons and preserving auditory nerve function. These findings suggest that hydrogen gas therapy may represent a novel therapeutic approach for treating hearing impairment in patients with auditory neuropathy by mitigating oxidative stress-related neuronal damage.
Plain-Language Summary
Researchers created hearing loss in gerbils by damaging the auditory nerve (the nerve that carries sound signals to the brain) while leaving the inner ear hair cells intact. They then treated some animals by having them breathe hydrogen gas at different concentrations. The hydrogen gas treatment reduced nerve cell death and preserved hearing function, suggesting that hydrogen may protect nerve cells from damage caused by oxidative stress (harmful chemical reactions in cells).
Abstract
Aim: Auditory neuropathy (AN) is a hearing disorder characterized by abnormal auditory nerve function with preservation of normal cochlear hair cells. This study was designed to investigate whether treatment with molecular hydrogen (H(2)), which can remedy damage in various organs via reducing oxidative stress, inflammation and apoptosis, is beneficial to ouabain-induced AN in gerbils. Methods: AN model was made by local application of ouabain (1 mmol/L, 20 mL) to the round window membrane in male Mongolian gerbils. H(2) treatment was given twice by exposing the animals to H(2) (1%, 2%, and 4%) for 60 min at 1 h and 6 h after ouabain application. Before and 7 d after ouabain application, the hearing status of the animals was evaluated using the auditory brainstem response (ABR) approach, the hear cell function was evaluated with distortion product otoacoustic emissions (DPOAE). Seven days after ouabain application, the changes in the cochleae, especially the spiral ganglion neurons (SGNs), were morphologically studied. TUNEL staining and immunofluorescent staining for activated caspase-3 were used to assess the apoptosis of SGNs. Results: Treatment with H(2) (2% and 4%) markedly attenuated the click and tone burst-evoked ABR threshold shift at 4, 8, and 16 kHz in ouabain-exposed animals. Neither local ouabain application, nor H(2) treatment changed the amplitude of DPOAE at 4, 8, and 16 kHz. Morphological study showed that treatment with H(2) (2%) significantly alleviated SGN damage and attenuated the loss of SGN density for each turn of cochlea in ouabain-exposed animals. Furthermore, ouabain caused significantly higher numbers of apoptotic SGNs in the cochlea, which was significantly attenuated by the H(2) treatment. However, ouabain did not change the morphology of cochlear hair cells. Conclusion: The results demonstrate that H(2) treatment is beneficial to ouabain-induced AN via reducing apoptosis. Thus, H(2) might be a potential agent for treating hearing impairment in AN patients.
DOI: 10.1038/aps.2011.190
