The influence of genetic variation in oxidative stress genes on human noise susceptibility

Hear Res. 2005 Apr;202(1-2):87-96. doi: 10.1016/j.heares.2004.09.005.

Abstract

Noise induced hearing loss (NIHL) is a complex disease caused by an interaction between genetic and environmental factors. Damage in the cochlea as a result of noise exposure appears to be mediated by reactive oxygen species (ROS). To investigate whether genetic variation in the human protective antioxidant system is associated with high or low susceptibility to NIHL, genetic polymorphisms derived from genes involved in the oxidative stress response were analysed in the 10% most susceptible and 10% most resistant extremes of 1200 Swedish noise-exposed workers. The genetic polymorphisms included 2 deletion polymorphisms for the GSTM1 and GSTT1 gene, and 14 SNPs derived from the CAT, SOD, GPX, GSR and GSTP1 genes. No significant differences were found between susceptible and resistant groups, providing no support for a major role of genetic variation of antioxidant enzymes in the susceptibility to NIHL.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Audiometry
  • Gene Deletion
  • Genetic Predisposition to Disease*
  • Genetic Variation*
  • Glutathione S-Transferase pi
  • Glutathione Transferase / genetics
  • Hearing Loss, Noise-Induced / genetics*
  • Humans
  • Isoenzymes / genetics
  • Oxidative Stress / genetics*
  • Oxidoreductases / genetics
  • Polymorphism, Single Nucleotide

Substances

  • Isoenzymes
  • Oxidoreductases
  • GSTP1 protein, human
  • Glutathione S-Transferase pi
  • Glutathione Transferase
  • glutathione S-transferase M1
  • glutathione S-transferase Mu 2