Authors
Kevin K Ohlemiller, Sandra L McFadden, Da-Lian Ding, Dorothy G Flood, Andrew G Reaume, Eric K Hoffman, Richard W Scott, James S Wright, Girish V Putcha, Richard J Salvi
Publication date
1999/10/1
Journal
Audiology and Neurotology
Volume
4
Issue
5
Pages
237-246
Publisher
S. Karger AG
Description
Reactive oxygen species (ROS) such as superoxide, peroxide and hydroxyl radicals are generated during normal cellular metabolism and are increased in acute injury and in many chronic disease states. When their production is inadequately regulated, ROS accumulate and irreversibly damage cell components, causing impaired cellular function and death. Antioxidant enzymes such as superoxide dismutase (SOD) play a vital role in minimizing ROS levels and ROS-mediated damage. The cytosolic form of Cu/Zn-SOD appears specialized to remove superoxide produced as a result of injury.‘Knockout’mice with targeted deletion of Sod1, the gene that codes for Cu/Zn-SOD, develop normally but show enhanced susceptibility to central nervous system injury. Since loud noise is injurious to the cochlea and is associated with elevated cochlear ROS, we hypothesized that Sod1 knockout mice would be more …
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