Abstract
Reactive oxygen species (ROS) generation is one of the mechanisms underlying noise-induced hearing loss (NIHL). Manganese superoxide dismutase (Mn-SOD), an antioxidant enzyme acting within the mitochondria, converts toxic superoxide to hydrogen peroxide. We investigated the role of Mn-SOD in NIHL by examining the extent of hearing loss and hair cell damage after noise exposure in C57BL/6 wild-type (WT) mice and Mn-SOD heterozygous knockout (HET) mice (n=6 each). Both HET and WT mice were exposed to 120dB sound pressure level at 4kHz octave band noise for 4h. Auditory brainstem responses (ABRs) were used to evaluate hearing thresholds before noise exposure, and at 1h, and 1, 3, 7, and 14days after exposure. The mice were euthanized 14days after noise exposure for examination of the cochlear pathology. Mean ABR thresholds were similarly elevated at all frequencies in both groups 1h after noise exposure, but were significantly worse, particularly at 4kHz, on post-noise exposure days 7 and 14 in HET mice compared with WT mice. Outer hair cell damage was significantly greater in all cochlear turns in HET mice compared with WT mice. Collectively, these findings suggest that Mn-SOD plays an important role in protecting the cochlea from noise-induced damage.
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