Male Sprague-Dawley rats were treated either with 1,2-diethylbenzene (1,2-DEB) or its putative active metabolite, 1,2-diacetylbenzene (1 ,2-DAB). Experimental rats and appropriate controls were examined electrophysiologically for brainstem auditory evoked potentials (BAEP). Oral administration of 1,
Diethylbenzene inhalation-induced electrophysiological deficits in peripheral nerves and changes in brainstem auditory evoked potentials in rats
✍ Scribed by F. Gagnaire; M. N. Becker; B. Marignac; P. Bonnet; J. de Ceaurriz
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 593 KB
- Volume
- 12
- Category
- Article
- ISSN
- 0260-437X
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✦ Synopsis
Abstract
Motor and sensory conduction velocities (MCV and SCV), amplitude of the sensory action potential (ASAP) of the tail nerve and parameters of brainstem auditory evoked potentials (BAEP) were studied in male Sprague‐Dawley rats after prolonged inhalation exposure to a commercial isomer mixture of diethylbenzene (DEB mixture) containing 6% 1, 2‐DEB. The MCV, SCV and ASAP were studied in one control group (10 rats) and three groups of 12 rats exposed to 500, 700 or 900 ppm DEB mixture for 6 h daily, 5 days per week, for 18 weeks. Rats used for recording BAEP (one control group and two other groups of 15 rats) were exposed to 600 and 800 ppm DEB mixture. The exposure time was the same.
Rats exposed to DEB mixture exhibited a time‐ and concentration‐dependent decrease in MCV, SCV and ASAP and a time‐ and concentration‐dependent increase of both the peak latencies of all BAEP components and the interpeak (I–V) differences.
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