Bibliographic Details
| Title: |
Pathogenesis and New Pharmacological Approaches to Noise-Induced Hearing Loss: A Systematic Review. |
| Authors: |
Santaolalla Sanchez, Francisco Javier, Gutierrez Posso, Juan David, Santaolalla Montoya, Francisco, Zabala, Javier Aitor, Arrizabalaga-Iriondo, Ane, Revuelta, Miren, Sánchez del Rey, Ana |
| Source: |
Antioxidants; Sep2024, Vol. 13 Issue 9, p1105, 30p |
| Subject Terms: |
NOISE-induced deafness, ACOUSTIC trauma, REACTIVE oxygen species, INNER ear, HAIR cells |
| Abstract: |
Noise-induced hearing loss (NIHL) is responsible for significant adverse effects on cognition, quality of life and work, social relationships, motor skills, and other psychological aspects. The severity of NIHL depends on individual patient characteristics, sound intensity, and mainly the duration of sound exposure. NIHL leads to the production of a reactive oxygen (ROS) inflammatory response and the activation of apoptotic pathways, DNA fragmentation, and cell death. In this situation, antioxidants can interact with free radicals as well as anti-apoptotics or anti-inflammatory substances and stop the reaction before vital molecules are damaged. Therefore, the aim of this study was to analyze the effects of different pharmacological treatments, focusing on exogenous antioxidants, anti-inflammatories, and anti-apoptotics to reduce the cellular damage caused by acoustic trauma in the inner ear. Experimental animal studies using these molecules have shown that they protect hair cells and reduce hearing loss due to acoustic trauma. However, there is a need for more conclusive evidence demonstrating the protective effects of antioxidant/anti-inflammatory or anti-apoptotic drugs' administration, the timeline in which they exert their pharmacological action, and the dose in which they should be used in order to consider them as therapeutic drugs. Further studies are needed to fully understand the potential of these drugs as they may be a promising option to prevent and treat noise-induced hearing loss. [ABSTRACT FROM AUTHOR] |
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| Database: |
Complementary Index |
