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of sensorineural hearing damage caused by exposure to noise.
Stimulation with sound of high intensity alters outer hair cell
plasma membrane fluidity. Prestin, the motor protein in the
outer hair cells, generates electromotility and the absence of
prestin results in the lack of electromotility and hearing loss.1?3
Otolin?1 is a secreted glycoprotein; its mRNA expression is
restricted to the vestibular maculae, semicircular canal cristae,
organ of Corti, and marginal cells of the stria vascularis.4 Its
functions include interaction with other inner ear proteins such
as prestin to maintain inner ear function,5 so they can serve
as circulatory biomarkers for NIHL.
Overstimulation of tissues by noise causes excess production of
reactive oxygen species (ROS), which oxidize cellular targets
such as proteins and DNA. The 8?hydroxy?2′?deoxyguanosine
(8?OHdG) DNA damage caused by ROS – that leads to
transversion mutation – is the most common form of oxidative
damage to DNA. DNA damage to cochlear hair cells is
essential for the development of NIHL. The activity of ROS
is antagonized by protective enzymes as human 8?OHdG
DNA glycosylase 1 (hOGG1) – an important enzyme in the
base excision repair pathway that eliminates 8?oxoG. Previous
studies have suggested that the Ser326Cys polymorphism in
exon 7 of hOGG1 gene may affect the enzyme activity so it
may be NIHL susceptibility genes.6
Therefore, we have undertaken this study to investigate the role
of prestin and otolin?1 in cochlear dysfunction in NIHL, test the

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