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12 WEEK EXPOSURE TO CARBONYL SULFIDE PRODUCES BRAIN LESIONS AND CHANGES IN BRAINSTEM AUDITORY (BAER) AND SOMATOSENAORY (SEP) EVOKED POTENTIALS IN FISCHER 344N RATS
Citation:
Herr, D W., J. E. Graff, P. B. Little, N. George, D. L. Morgan, AND R. C. Sills. 12 WEEK EXPOSURE TO CARBONYL SULFIDE PRODUCES BRAIN LESIONS AND CHANGES IN BRAINSTEM AUDITORY (BAER) AND SOMATOSENAORY (SEP) EVOKED POTENTIALS IN FISCHER 344N RATS. Presented at Society of Toxicology, Salt Lake City, UT, 3/9-13/2003.
Description:
Carbonyl sulfide (COS) is a chemical intermediate in the production of pesticides and herbicides, is a metabolite of carbon disulfide, is produced by the combustion of organic material, and is found occurring in nature. COS was included in a Toxic Substances Control Act request for data, and has been listed as a Clean Air Act hazardous air pollutant. To examine possible neurotoxicity of COS, male and female Fischer 344N rats were exposed by inhalation to 0, 200, 300, or 400 ppm COS for 6 h/day, 5 days/week, for 12 weeks. After the final exposure, the animals were allowed to recover for about 42 days. Subjects were surgically implanted with screw electrodes over the forelimb/facial and hindlimb/tail somatosensory cortex and the cerebellum, and allowed to recover for one week. Unanesthetized animals were placed in a restrainer and presented with electrical stimuli (1, 2, 3 mA biphasic square wave presented at 0.9 Hz) to the ventral caudal tail nerve to record somatosensory potentials (SEPs). Auditory stimuli consisted of rarefaction clicks and pure tone pips (4, 16, 64 kHz presented at 5.6 Hz) using three intensities (50, 65, 80 dB SPL; 65, 70, 80 dB SPL for 64 kHz). Exposure to COS produced a lesion in the lateral frontal/parietal cortex in a subset of the 400 ppm group. In the animals with the lesion there was an increase in SEP amplitude recorded from the forelimb/facial (but not the hindlimb/tail) somatosensory cortex. Exposure to COS decreased BAER amplitudes (peak P3 and P4 region), and histopathology confirmed the presence of brainstem lesions in the superior olivary complex and inferior colliculus. Thus, exposure of rats to COS resulted in changes in auditory and somatosensory physiology and produced brain lesions in regions associated with the neural generators of these physiological measures. This is an abstract of a proposed presentation and does not necessarily reflect EPA policy.