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Olfactory Mucosal Necrosis in Male CD Rats Following Acute Inhalation Exposure to Hydrogen Sulfide: Reversibility and the Possible Role of Regional Metabolism

CT Centers for Health Research, Research Triangle Park, North Carolina 27709

David F. Meleason

CT Centers for Health Research, Research Triangle Park, North Carolina 27709

Madhabananda Sar

CT Centers for Health Research, Research Triangle Park, North Carolina 27709

Marianne W. Marshall

CT Centers for Health Research, Research Triangle Park, North Carolina 27709

R. Arden James

CT Centers for Health Research, Research Triangle Park, North Carolina 27709

Elizabeth A. Gross

CT Centers for Health Research, Research Triangle Park, North Carolina 27709

Joseph T. Martin

CT Centers for Health Research, Research Triangle Park, North Carolina 27709

David C. Dorman

CT Centers for Health Research, Research Triangle Park, North Carolina 27709, dorman{at}ciit.org

Hydrogen sulfide (H ₂S) 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 H₂S for 3 hours/day for 1 or 5 days consecutively. The nose was histologically examined 24 hours after H₂S 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 ₂S 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 H₂S 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 H₂S than in regions that were not. These findings demonstrate that acute exposure to 80 ppm H₂S resulted in reversible lesions in the respiratory and olfactory mucosae of the CD rat and that CO immunoreactivity may be a susceptibility factor for H₂S-induced olfactory toxicity in the rat.

Key Words: Nasal pathology • cytochrome oxidase • annexin I • olfactory marker protein • immunohistochemistry • microvillar cells • mitochondrial swelling • olfactory epithelial regeneration.

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