Version 1
: Received: 21 July 2020 / Approved: 22 July 2020 / Online: 22 July 2020 (07:58:12 CEST)
How to cite:
Park, D.J.; Ha, S.; Choi, J.S.; Lee, S.H.; Park, J.; Seo, Y.J. Induced Short-term Hearing Loss due to Stimulation of Age-related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection. Preprints2020, 2020070505 (doi: 10.20944/preprints202007.0505.v1).
Park, D.J.; Ha, S.; Choi, J.S.; Lee, S.H.; Park, J.; Seo, Y.J. Induced Short-term Hearing Loss due to Stimulation of Age-related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection. Preprints 2020, 2020070505 (doi: 10.20944/preprints202007.0505.v1).
Cite as:
Park, D.J.; Ha, S.; Choi, J.S.; Lee, S.H.; Park, J.; Seo, Y.J. Induced Short-term Hearing Loss due to Stimulation of Age-related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection. Preprints2020, 2020070505 (doi: 10.20944/preprints202007.0505.v1).
Park, D.J.; Ha, S.; Choi, J.S.; Lee, S.H.; Park, J.; Seo, Y.J. Induced Short-term Hearing Loss due to Stimulation of Age-related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection. Preprints 2020, 2020070505 (doi: 10.20944/preprints202007.0505.v1).
Abstract
Age-related hearing loss (ARHL) is the most common sensory disorder in the elderly. It is associated with aging and hair cell death due to oxidative stress-induced mitochondrial dysfunction. Although transgenic mice and long-term cultures for induction of aging have been used to study ARHL, there are presently no ARHL animal models stimulated by intermittent environmental change for aging. In this study, an ARHL animal model was established by inducing continuous oxidative stress to promote short-term aging of cells, determined based on the expression of the hearing loss-induced phenotype and aging related factors in the short term. The incidence of hearing loss was significantly different among the groups subjected to intermittent hypoxic environment, high-fat diet (HFD), and injection with D-galactose. Continuous oxidative stress and HFD were factors that accelerated cellular aging. Increase in UCP2 affected oxidative stress and mitochondrial dysfunction. CDH23, SLC26A4, KCNQ4, Myo7a, and Myo6, which are ARHL-related factors, were modified by oxidative stress in cells of the hearing organ. We found that intermittent hypoxic, HFD, and galactose injection accelerated cellular aging in the short term. Thus, we anticipate that the development of this hearing loss animal model, which reflects intermittent environmental changes, will benefit future research on ARHL.
Subject Areas
mitochondria dysfunction; reactive oxygen species; hypoxic; D-galactose; high fat diet; aging; hearing loss; mechanisms of hearing loss
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Dong Jun Park
Sunmok Ha