Oxidative DNA damage is associated with intense noise exposure in the rat.
Van Campen-L; Murphy-W; Franks-J; Mathias-P; Toraason-M
Hear Res 2002 Feb; 164(1-2):29-38
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 (8OHdG) 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. 8OHdG 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.
Noise-induced-hearing-loss; Antioxidants; Noise-exposure; Animal-studies; Animals; DNA-damage; Lipid-peroxidation; Aldehydes; Auditory-system; Brain-disorders; Liver-disorders
Engineering and Physical Hazards Branch, Division of Applied Research and Technology, National Institute for Occupational Safety and Health, Cincinnati, OH 45226, USA