Effect of SOD1 overexpression on age- and noise-related hearing loss

Free Radic Biol Med. 2003 Apr 1;34(7):873-80. doi: 10.1016/s0891-5849(02)01439-9.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Age Factors
  • Aging
  • Animals
  • DNA, Mitochondrial / genetics
  • Free Radicals
  • Gene Deletion
  • Hearing Loss / genetics*
  • Hearing Loss, Noise-Induced / genetics*
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Noise
  • Oxidative Stress
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase / metabolism*
  • Time Factors
  • Tissue Distribution


  • DNA, Mitochondrial
  • Free Radicals
  • Superoxide Dismutase