期刊
HEARING RESEARCH
卷 164, 期 1-2, 页码 29-38出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/S0378-5955(01)00391-4
关键词
free radical; reactive oxygen species; oxidative stress; cochlea; DNA; 8-hydroxy-2 '-deoxyguanosine; thiobarbituric acid-reactive substance
Increasing evidence suggests that noise-induced hearing loss may be reduced or prevented with antioxidant therapy. Biochemical markers of reactive oxygen species (ROS)-induced damage can help elucidate possible treatment timing constraints. This study examined the time course of ROS damage following a 2-h, broad-band noise exposure resulting in permanent threshold shift in 35 Long-Evans rats. Cochlea, brain, liver, serum and urine were analyzed at 1, 3, 8, 72, and 672 h (28 days) after exposure. Oxidative DNA damage was assessed by measuring 8-hydroxy-2'-deoxyguanosine (80HdG) by high performance liquid chromatography with electrochemical detection. Lipid peroxidation was measured via the thiobarbituric acid-reactive substances (TBARS) colorimetric assay for detection of aldehydes (e.g., malondialdehyde). Auditory brainstem. response and distortion product otoacoustic emission thresholds showed progressive elevation for the 3- and 8-h groups, then notable recovery for the 72-h group, and some worsening for the 672-h group. 80HdG was significantly elevated in cochlea in the 8-h group, and in brain and liver for the 72-h group. TBARS were significantly elevated in serum for the 72-h group. Based upon oxidative DNA damage present in cochlea following intense noise, we postulate that the first 8 h following exposure might be a critical period for antioxidant treatment. Published by Elsevier Science B.V.
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