The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
Cytochrome Oxidase Inhibition Induced by Acute Hydrogen Sulfide Inhalation: Correlation with Tissue Sulfide Concentrations in the Rat Brain, Liver, Lung, and Nasal Epithelium
Abstract
Hydrogen sulfide (H2S) is an important brain, lung, and nose toxicant. Inhibition of cytochrome oxidase is the primary biochemical effect associated with lethal H2S exposure. The objective of this study was to evaluate the relationship between the concentration of sulfide and cytochrome oxidase activity in target tissues following acute exposure to sublethal concentrations of inhaled H2S. Hindbrain, lung, liver, and nasal (olfactory and respiratory epithelial) cytochrome oxidase activity and sulfide concentrations were determined in adult male CD rats immediately after a 3-h exposure to H2S (10, 30, 80, 200, and 400 ppm). We also determined lung sulfide and sulfide metabolite concentrations at 0, 1.5, 3, 3.25, 3.5, 4, 5, and 7 h after the start of a 3-h H2S exposure to 400 ppm. Lung sulfide concentrations increased during H2S exposure and rapidly returned to endogenous levels within 15 min after the cessation of the 400-ppm exposure. Lung sulfide metabolite concentrations were transiently increased immediately after the end of the 3-h H2S exposure. Decreased cytochrome oxidase activity was observed in the olfactory epithelium following exposure to > or = 30 ppm H2S. Increased olfactory epithelial sulfide concentrations were observed following exposure to 400 ppm H2S. Hindbrain and nasal respiratory epithelial sulfide concentrations were unaffected by acute H2S exposure. Nasal respiratory epithelial cytochrome oxidase activity was reduced following acute exposure to > or = 30 ppm H2S. Liver sulfide concentrations were increased following exposure to > or = 200 ppm H2S and cytochrome oxidase activity was increased following inhalation exposure to > or = 10 ppm H2S. Our results suggest that cytochrome oxidase inhibition is a sensitive biomarker of H2S exposure in target tissues, and sulfide concentrations are unlikely to increase postexposure in the brain, lung, or nose following a single 3-h exposure to < or = 30 ppm H2S.
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“Acute administration of hydrogen sulfide (H2S) into airway can induce cytochrome oxidase inhibition in the animal brain, impairing mitochondrial function [57].”
From Healthy Human Fecal Microbiota Transplantation into Mice Attenuates MPTP-Induced Neurotoxicity via AMPK/SOD2 Pathway (2023) · cites this paper as [57]
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Hydrogen sulphide and its therapeutic potential
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Hydrogen Sulfide as Endothelium-Derived Hyperpolarizing Factor Sulfhydrates Potassium Channels
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Metadata
- Authors
- Dorman, D. C.
- Affiliations
- Bristol-Myers Squibb (United States) (US)
- Corresponding author
- Dorman, D. C.
- ORCID
- Dorman, D. C.
- Venue
- Toxicological Sciences
- Publisher
- Oxford University Press (OUP)
- Published
- 2002-01-01
- Volume
- 65
- Issue
- 1
- Pages
- 18-25
- ISSN
- 1096-0929 (ISSN-L)
- OpenAlex
- W2172247722
- Cited by
- 362
- References
- 56
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 7 · 2023: 13 · 2022: 13 · 2021: 10 · 2020: 16 · 2019: 18 · 2018: 21 · 2017: 22 · 2016: 17 · 2015: 34 · 2014: 19 · 2013: 15 · 2012: 28
- FWCI
- 3.50
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Toxicological Sciences (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Sulfur Compounds in Biology
- Health Sciences › Medicine › Emergency Medicine › Poisoning and overdose treatments
- Health Sciences › Medicine › Physiology (medical) › Biomedical and Chemical Research
- Keywords
- hydrogen sulfide, cytochrome c oxidase inhibition, acute inhalation exposure, sulfide concentration, olfactory epithelium, nasal respiratory epithelium, hindbrain, liver, lung, biomarkers of exposure, sublethal exposure
- MeSH terms
- Animals, Brain, Electron Transport Complex IV, Hydrogen Sulfide, Liver, Lung, Male, Nasal Mucosa, Sulfates, Thiosulfates, Time Factors, Inhalation Exposure, Toxicity Tests, Acute, Rats
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