AI Article Synopsis
- Reactive oxygen species (ROS) are linked to hearing loss caused by aging and noise exposure, with superoxide dismutases (SODs) acting as a defense against ROS damage.
- The absence of the Cu/Zn SOD (SOD1) worsens hearing loss from noise and aging, while overexpressing SOD1 was thought to protect against these losses.
- However, research using transgenic mice with the human SOD1 gene found no protective effects against age-related or noise-induced hearing loss, suggesting that oxidative metabolism in the cochlea is more complex than previously thought.
Article Abstract
Reactive oxygen species (ROS) have been implicated in hearing loss associated with aging and noise exposure. Superoxide dismutases (SODs) form a first line of defense against damage mediated by the superoxide anion, the most common ROS. Absence of Cu/Zn SOD (SOD1) has been shown to potentiate hearing loss related to noise exposure and age. Conversely, overexpression of SOD1 may be hypothesized to afford a protection from age- and noise-related hearing loss. This hypothesis may be tested using a transgenic mouse model carrying the human SOD1 gene. Contrary to expectations, here, we report that no protection against age-related hearing loss was observed in mice up to 7 months of age or from noise-induced hearing loss when 8 week old mice were exposed to broadband noise (4-45 kHz, 110 dB for 1 h). Mitochondrial DNA deletion, an index of aging, was elevated in the acoustic nerve of transgenic mice compared to nontransgenic littermates. The results indicate the complexity of oxidative metabolism in the cochlea is greater than previously hypothesized.
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| http://dx.doi.org/10.1016/s0891-5849(02)01439-9 | DOI Listing |
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