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Sensorineural hearing loss is the most common sensory deficit. The etiologies of sensorineural hearing loss have been described and can be congenital or acquired. For congenital non-syndromic hearing loss, mutations that are related to sites of cochlear damage have been discovered (e.g., connexin proteins, mitochondrial genes, etc.). For cytomegalovirus infection or auditory neuropathies, mechanisms are also well known and well researched. Although the etiologies of sensorineural hearing loss may be evident for some patients, the damaged sites and pathological mechanisms remain unclear for patients with progressive post-lingual hearing loss. Metabolomics is an emerging technique in which all metabolites present in a sample at a given time are analyzed, reflecting a physiological state. The objective of this study was to review the literature on the use of metabolomics in hearing loss. The findings of this review suggest that metabolomic studies may help to develop objective tests for diagnosis and personalized treatment.

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The pathophysiological mechanisms of noise-induced hearing loss remain unknown. Identifying biomarkers of noise-induced hearing loss may increase the understanding of pathophysiological mechanisms of deafness, allow for a more precise diagnosis, and inform personalized treatment. Emerging techniques such as metabolomics can help to identify these biomarkers. The objective of the present study was to investigate immediate-early changes in the perilymph metabolome following acoustic trauma. Metabolomic analysis was performed using liquid chromatography coupled to mass spectrophotometry to analyze metabolic changes in perilymph associated with noise-induced hearing loss. Sheep (n = 6) were exposed to a noise designed to induce substantial hearing loss. Perilymph was collected before and after acoustic trauma. Data were analyzed using univariate analysis and a supervised multivariate analysis based on partial least squares discriminant analysis. A metabolomic analysis showed an abundance of 213 metabolites. Four metabolites were significantly changed following acoustic trauma (Urocanate (p = 0.004, FC = 0.48), S-(5’-Adenosyl)-L-Homocysteine (p = 0.06, FC = 2.32), Trigonelline (p = 0.06, FC = 0.46) and N-Acetyl-L-Leucine (p = 0.09, FC = 2.02)). The approach allowed for the identification of new metabolites and metabolic pathways involved with acoustic trauma that were associated with auditory impairment (nerve damage, mechanical destruction, and oxidative stress). The results suggest that metabolomics provides a powerful approach to characterize inner ear metabolites which may lead to identification of new therapies and therapeutic targets.