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Tissue Eng Regen Med ; 20(5): 779-787, 2023 08.
Article in English | MEDLINE | ID: mdl-37294515

ABSTRACT

BACKGROUND: 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. METHODS: 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). RESULTS: 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. CONCLUSION: 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.


Subject(s)
Galactose , Presbycusis , Mice , Animals , Galactose/adverse effects , Disease Models, Animal , Mice, Inbred C57BL , Presbycusis/chemically induced , Presbycusis/genetics , Presbycusis/metabolism , Superoxide Dismutase , Hypoxia
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