Original Contribution Elevation of superoxide dismutase increases acoustic trauma from noise exposure

AbstractThe 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 exposurecaused 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 ofsaline-treated animals. Likewise, transgenic mice overexpressing SOD1 tended to suffer higher threshold shifts than nontransgenic littermatesfrom noise exposure. The findings indicate that increasing SOD1 enhances auditory dysfunction following noise exposure.D 2004 Elsevier Inc. All rights reserved. Keywords: Reactive oxygen species; Hearing loss; Acoustic trauma; Redox regulation; SOD; Free radicals