Abstract:
:Mutations in mitochondrial DNA (mtDNA) are associated with diverse pathological states in humans, notably sensorineural deafness. In humans, mtDNA4977 deletion, known as common deletion, is thought to play a critical role in presbyacusis. A similar mtDNA deletion occurs in the naturally aging rats is mtDNA4834 deletion. Today, it is still obscure about the effect of common mtDNA deletion on the presbyacusis and hearing loss. We establish a model of rat associated with mtDNA4834 deletion in inner ear by d-galactose. It was found that the malondialdehyde (MDA) increased with superoxide dismutase (SOD) decreasing in the inner ear of the rat treated with d-galactose than of the control. However, there was no significant difference in elevation of ABR threshold between the rat with mtDNA4834 deletion induced by d-galactose and control. After aminoglycoside antibiotic injected, the hearing threshold of the rats carrying mtDNA4834 deletion increased significantly compared with the rats without mtDNA4834 deletion. The results show that resembled accelerated aging in the inner ear of the rat could be induced by injecting d-galactose. Moreover, those suggest that mtDNA4834 deletion can not directly induce the hearing loss, but acting as a predisposing factor which can greatly enhance the sensitivity of the inner ear to the aminoglycoside antibiotic.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Kong WJ,Hu YJ,Wang Q,Wang Y,Han YC,Cheng HM,Kong W,Guan MXdoi
10.1016/j.bbrc.2006.03.060subject
Has Abstractpub_date
2006-05-26 00:00:00pages
425-30issue
1eissn
0006-291Xissn
1090-2104pii
S0006-291X(06)00563-8journal_volume
344pub_type
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