In:
Toxicologic Pathology, SAGE Publications, Vol. 30, No. 2 ( 2002-02), p. 200-208
Kurzfassung:
Hydrogen sulfide (H 2 S) is a potent inhibitor of cytochrome oxidase (CO) and is associated with dysosmia and anosmia in humans and nasal lesions in exposed rodents. An improved understanding of the pathogenesi s of these lesions is needed to determine their toxicological relevance. We exposed 10-week-old male CD rats to 0, 30, 80, 200, or 400 ppm H 2 S for 3 hours/day for 1 or 5 days consecutively. The nose was histologically examined 24 hours after H 2 S exposure, and lesion recovery was assessed at 2 and 6 weeks following the 5-day exposure. A single 3-hour exposure to ≥80 ppm H 2 S resulted in regeneration of the respiratory mucosa and full thickness necrosis of the olfactory mucosa localized to the ventral and dorsal meatus, respectively. Repeated exposure to the same concentrations caused necrosis of the olfactory mucosa with early mucosal regeneration that extended from the dorsal medial meatus to the caudal regions of the ethmoid recess. Acute exposure to 400 ppm H 2 S induced severe mitochondrial swelling in sustentacular cells and olfactory neurons, which progressed to olfactory epithelial necrosis and sloughing. CO immunoreactive cells were more frequently observed in regions of the olfactory mucosa commonly affected by H 2 S than in regions that were not. These findings demonstrate that acute exposure to ≥80 ppm H 2 S resulted in reversible lesions in the respiratory and olfactory mucosae of the CD rat and that CO immunoreactivity may be a susceptibility factor for H 2 S-induced olfactory toxicity in the rat.
Materialart:
Online-Ressource
ISSN:
0192-6233
,
1533-1601
DOI:
10.1080/019262302753559533
Sprache:
Englisch
Verlag:
SAGE Publications
Publikationsdatum:
2002
ZDB Id:
2056753-4
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