Abstract
Using senescence marker protein 30 (SMP30)/gluconolactonase (GNL) knockout (KO) mice, which cannot synthesize vitamin C (VC), we examined whether modulating VC level affects age-related hearing loss (AHL). KO and wild-type (WT) C57BL/6 mice were given water containing 1.5 g/L VC [VC(+)] or 37.5 mg/L VC [VC(-)]. At 10 months of age, KO VC(-) mice showed significant reduction in VC level in the inner ear, plasma, and liver, increase in auditory brainstem response (ABR) thresholds, and decrease in the number of spiral ganglion cells compared to WT VC(-), WT VC(+), and KO VC(+) mice. There were no differences in VC level in the inner ear, ABR thresholds, or the number of spiral ganglion cells among WT VC(-), WT VC(+), and KO VC(+) mice. These findings suggest that VC depletion can accelerate AHL but that supplementing VC may not increase VC level in the inner ear or slow AHL in mice.
Original language | English |
---|---|
Pages (from-to) | 394-398 |
Number of pages | 5 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 390 |
Issue number | 3 |
DOIs | |
Publication status | Published - 2009 Dec 18 |
Externally published | Yes |
Keywords
- Aging
- Ascorbic acid
- Cochlea
- Gluconolactonase
- Hearing loss
- Oxidative stress
- Senescence marker protein 30
- Vitamin C
ASJC Scopus subject areas
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology