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Effect of superoxide dismutase and allopurinol on impulse noise-exposed guinea pigs--electrophysiological and biochemical study
Objective: To investigate the protective effect of two anti-reactive oxygen species (ROS) substances, copper-zinc superoxide dismutase (CuZn-SOD) and allopurinol, in impulse noise-exposed guinea pigs. Material and Methods: Allopurinol or CuZn-SOD were administered intraperitoneally before exposure t...
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Published in: | Acta oto-laryngologica 2003-07, Vol.123 (7), p.802-807 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Objective: To investigate the protective effect of two anti-reactive oxygen species (ROS) substances, copper-zinc superoxide dismutase (CuZn-SOD) and allopurinol, in impulse noise-exposed guinea pigs.
Material and Methods: Allopurinol or CuZn-SOD were administered intraperitoneally before exposure to 125 dB SPL noise centered at 2.0-3.0 kHz, with a repetition rate of 4/s, for 1.8 h. Hearing thresholds were tested by means of electrocochleography after implanting the animals with permanent electrodes. The presence of lipoperoxides in the guinea pig cochleae exposed to noise-induced oxidative stress was determined by means of the dosage of malondialdhyde, evaluated by measuring the content of thiobarbituric acid reactive substances in perilymph samples.
Results: Acoustic stress induced ROS formation and both allopurinol and CuZn-SOD exerted a protective effect on the cochlea. Comparison of compound action potential thresholds in different animal groups showed that the temporary threshold shift was significantly lower in treated animals than in those without pharmacological protection.
Conclusion: The protective effect of the antioxidant agents demonstrates that, even at a high level of impulse noise exposure, a metabolic mechanism of cochlear damage may still play an important role in noise-exposed sensorineural hearing loss. |
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ISSN: | 0001-6489 1651-2251 |
DOI: | 10.1080/00016480310005138 |