Elevation of superoxide dismutase increases acoustic trauma from noise exposure.
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.
Endo
Tsuyoshi
T
Department of Otolaryngology-Head and Neck Surgery, Graduate School of Medicine, Kyoto University, Kawaharacho 54, Shogoin, Sakyo-ku, 606-8507 Kyoto, Japan.
Nakagawa
Takayuki
T
Iguchi
Fukuichiro
F
Kita
Tomoko
T
Okano
Takayuki
T
Sha
Su-Hua
SH
Schacht
Jochen
J
Shiga
Atsushi
A
Kim
Tae-Soo
TS
Ito
Juichi
J
D000161:Acoustic Stimulation; D000818:Animals; D002374:Catalase / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009622:Noise / Q000009:adverse effects*; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism*; D020196:Trauma, Nervous System / Q000201:enzymology* / Q000235:genetics
D002374:Catalase; D013482:Superoxide Dismutase