D-Galactose and Hypoxia Induce the Early Onset of Age-Related Hearing Loss Deterioration in a Mouse Model
We previously showed that aging accelerates after 3 months of exposure to hypoxia and environmental change but not genetic modifications. Here, we aimed to simply induce early-onset age-related hearing loss within a short period based on our previous method. We randomly divided 16 C57BL/6 mice into...
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Published in | Tissue engineering and regenerative medicine Vol. 20; no. 5; p. 779 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Korea (South)
01.08.2023
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Subjects | |
Online Access | Get more information |
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Summary: | We previously showed that aging accelerates after 3 months of exposure to hypoxia and environmental change but not genetic modifications. Here, we aimed to simply induce early-onset age-related hearing loss within a short period based on our previous method.
We randomly divided 16 C57BL/6 mice into four groups that were maintained under conditions of normoxia and hypoxia with or without injected D-galactose for 2 months. Deteriorated hearing, the expression of age-related factors, and oxidative stress responses were detected using the click and tone burst auditory brainstem response test, reverse transcription-polymerase chain reaction, and by measuring superoxide dismutase (SOD).
The group maintained under hypoxia combined with D-galactose lost hearing particularly at 24 Hz and 32 Hz at 6 weeks compared with the other groups. Aging-related factors were also significantly decreased in the hypoxia and D-galactose groups. However, SOD levels did not significantly differ among the groups.
Age-related hearing loss is an environmental disorder induced by chronic oxidative stress associated with genetic backgrounds. Our findings suggested that D-galactose and hypoxia can induce the phenotypes of age-related hearing loss and aging-associated molecules in a murine model within a short time with environmental stimulation alone. |
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ISSN: | 2212-5469 |
DOI: | 10.1007/s13770-023-00547-8 |