Elevation of superoxide dismutase increases acoustic trauma from noise exposure

Tsuyoshi Endo, Takayuki Nakagawa, Fukuichiro Iguchi, Tomoko Kita, Takayuki Okano, Su Hua Sha, Jochen Schacht, Atsushi Shiga, Tae Soo Kim, Juichi Ito

Research output: Contribution to journalArticlepeer-review

29 Citations (Scopus)


The generation of superoxide has been implicated as a cause of cochlear damage from excessive noise. Cu/Zn superoxide dismutase (SOD1) generally will protect against superoxide-mediated tissue injury but protection by this enzyme against noise trauma is controversial. This study assessed auditory function in C57BL/6 mice overexpressing SOD1 or treated with lecithinized SOD1 (PC-SOD1). Noise exposure caused significantly higher threshold shifts in PC-SOD1-treated animals than physiological saline-treated animals. Cochlear tissues of PC-SOD1-treated animals exhibited significant elevation of the levels in the SOD activity, not in the catalase activity, in comparison with those of saline-treated animals. Likewise, transgenic mice overexpressing SOD1 tended to suffer higher threshold shifts than nontransgenic littermates from noise exposure. The findings indicate that increasing SOD1 enhances auditory dysfunction following noise exposure.

Original languageEnglish
Pages (from-to)492-498
Number of pages7
JournalFree Radical Biology and Medicine
Issue number4
Publication statusPublished - 15-02-2005
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Physiology (medical)


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