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• W3199590624 endingPage "150365" @default.
• W3199590624 startingPage "150365" @default.
• W3199590624 abstract "Hydrogen sulfide (H 2 S) is a highly toxic gas in many environmental and occupational places. It can induce multiple organ injuries particularly in lung, trachea and liver, but the relevant mechanisms remain poorly understood. In this study, we used a TMT-based discovery proteomics to identify key proteins and correlated molecular pathways involved in the pathogenesis of acute H 2 S-induced toxicity in porcine lung, trachea and liver tissues. Pigs were subjected to acute inhalation exposure of up to 250 ppm of H 2 S for 5 h for the first time. Changes in hematology and biochemical indexes, serum inflammatory cytokines and histopathology demonstrated that acute H 2 S exposure induced organs inflammatory injury and dysfunction in the porcine lung, trachea and liver. The proteomic data showed 51, 99 and 84 proteins that were significantly altered in lung, trachea and liver, respectively. Gene ontology (GO) annotation, KEGG pathway and protein-protein interaction (PPI) network analysis revealed that acute H 2 S exposure affected the three organs via different mechanisms that were relatively similar between lung and trachea. Further analysis showed that acute H 2 S exposure caused inflammatory damages in the porcine lung and trachea through activating complement and coagulation cascades, and regulating the hyaluronan metabolic process. Whereas antigen presentation was found in the lung but oxidative stress and cell apoptosis was observed exclusively in the trachea. In the liver, an induced dysfunction was associated with protein processing in the endoplasmic reticulum and lipid metabolism. Further validation of some H 2 S responsive proteins using western blotting indicated that our proteomics data were highly reliable. Collectively, these findings provide insight into toxic molecular mechanisms that could potentially be targeted for therapeutic intervention for acute H 2 S intoxication. • Acute H 2 S exposure affected porcine lung, trachea and liver tissues via different mechanisms. • The toxic mechanisms of acute H 2 S exposure in the lung and trachea are relatively similar. • Complement and coagulation cascades, antigen presentation and hyaluronan metabolism were implicated in lung. • Complement and coagulation cascades, oxidative stress, cell apoptosis and hyaluronan metabolism were implicated in trachea. • Acute H 2 S exposure induced liver dysfunction via affecting protein synthesis and lipid metabolism." @default.
• W3199590624 created "2021-09-27" @default.
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• W3199590624 date "2022-02-01" @default.
• W3199590624 modified "2023-09-25" @default.
• W3199590624 title "Quantitative proteomics reveals tissue-specific toxic mechanisms for acute hydrogen sulfide-induced injury of diverse organs in pig" @default.
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