文献类型： 外文期刊

作者： Liu, Zhen ¹ ; Chen, Liang ¹ ; Gao, Xin ³ ; Zou, Ruixia ⁴ ; Meng, Qingshi ¹ ; Fu, Qin ⁵ ; Xie, Yanjiao ¹ ; Miao, Qixiang ¹ ; Chen, Lei ¹ ; Tang, Xiangfang ¹ ; Zhang, Sheng ⁵ ; Zhang, Hongfu ¹ ; Schroyen, Martine ² ;

作者机构： 1.Chinese Acad Agr Sci, Inst Anim Sci, State Key Lab Anim Nutr, Beijing 100193, Peoples R China

2.Univ Liege, Precis Livestock & Nutr Unit, Gembloux Agrobio Tech, TERRA Teaching & Res Ctr, Passage Deportes 2, B-5030 Gembloux, Belgium

3.Chinese Acad Agr Sci, Lanzhou Vet Res Inst, State Key Lab Vet Etiol Biol, Lanzhou 730046, Peoples R China

4.Chinese Acad Agr Sci, Grad Sch, Beijing 100081, Peoples R China

5.Cornell Univ, Inst Biotechnol, Prote & Metabol Facil, Ithaca, NY 14853 USA

关键词： H2S; Acute exposure; TMT-based proteomics; Multi-organ injury; Porcine; Inflammatory injury

期刊名称：SCIENCE OF THE TOTAL ENVIRONMENT （ 影响因子：10.753； 五年影响因子：10.237 ）

ISSN： 0048-9697

年卷期： 2022 年 806 卷

页码：

收录情况： SCI

摘要： Hydrogen sulfide (H2S) 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 H2S-induced toxicity in porcine lung, trachea and liver tissues. Pigs were subjected to acute inhalation exposure of up to 250 ppm of H2S for 5 h for the first time. Changes in hematology and biochemical indexes, serum inflammatory cytokines and histopathology demonstrated that acute H2S 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 H2S exposure affected the three organs via different mechanisms that were relatively similar between lung and trachea. Further analysis showed that acute H2S 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 H2S 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 H2S intoxication. (C) 2021 Published by Elsevier B.V.