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Combined cell death of co-exposure to aldehyde mixtures on human bronchial epithelial BEAS-2B cells: Molecular insights into the joint action

文献类型：期刊论文

作者Zhang, Sen1,2,3; Zhang, Jingni1,2,3; Cheng, Wanyan1,3; Chen, Huan3; Wang, An1; Liu, Yong1; Hou, Hongwei3; Hu, Qingyuan3
刊名CHEMOSPHERE
出版日期2020-04-01
卷号244
关键词Formaldehyde Acrolein Combined action Cell death Apoptotic signaling pathway
ISSN号0045-6535
DOI10.1016/j.chemosphere.2019.125482
通讯作者Hou, Hongwei(houhw2015@163.com) ; Hu, Qingyuan(huqy1965@163.com)
英文摘要Aldehydes are common air pollutants and metabolites of the organism, which widely exist in many in vivo (e.g. Alzheimer's disease) and in vitro (e.g. cigarette smoke) situations. Individual aldehydes have been studied well alone, while their combined toxicity is still obscure. Here, we examined the combined apoptosis of aldehyde mixtures in BEAS-2B cells at smoking-related environmental/physiologically relevant concentrations, and the potential mechanism was investigated further based on the related signaling pathway. Co-exposure to aldehyde mixtures demonstrated significant synergistic interaction on apoptosis in a concentration-dependent manner, which differed from the expectation based on single aldehydes. Moreover, formaldehyde significantly potentiated the induction of death receptor-5, caspase 8/10, cleaved caspase 3/7/9, pro-apoptotic proteins (Bim, Bad and Bax), depolarization of MMP (mitochondrial membrane potential) and AIF (apoptosis-inducing factor) induced by acrolein, and synergistically decreased expressions of pro-survival proteins (Bcl-2 and Bcl-XL) and poly ADP-ribose polymerase. Therefore, aldehyde mixture-induced synergistic apoptosis was mediated both by TRAIL death receptor and mitochondrial pathway. Additionally, reactive oxygen species, Ca2+ levels, DNA damage, and phosphorylated MDM2 were all synergistically induced by aldehyde mixtures, while total p53, phosphorylated p53 and phosphorylated AKT (serine/threonine kinase) were inhibited. Antioxidants N-acetylcysteine suppressed the aldehyde mixture-induced ROS, DNA damage and apoptosis, and blocked the TRAIL death receptor and mitochondrial pathway, while it did not rescue the p53 and AKT pathway. Briefly, aldehyde mixtures induced synergistic apoptosis even at smoking-related environmental/physiologically relevant concentrations, which could be enhanced through ROS-mediated death receptor/mitochondria' pathway, and the down-regulation of phosphorylated AKT. (C) 2019 Elsevier Ltd. All rights reserved.
WOS关键词ACROLEIN INDUCES APOPTOSIS ; IN-VITRO ; RECEPTOR PATHWAY ; FORMALDEHYDE ; TOXICITY ; ACTIVATION ; EXPRESSION ; INDUCTION ; REPAIR ; SMOKE
WOS研究方向Environmental Sciences & Ecology
语种英语
WOS记录号WOS:000515197700055
出版者PERGAMON-ELSEVIER SCIENCE LTD
源URL[http://ir.hfcas.ac.cn:8080/handle/334002/103935]  
专题中国科学院合肥物质科学研究院
通讯作者Hou, Hongwei; Hu, Qingyuan
作者单位1.Chinese Acad Sci, Inst Appl Technol, Hefei Inst Phys Sci, Hefei 230031, Peoples R China
2.Univ Sci & Technol China, Hefei 230026, Peoples R China
3.China Natl Tobacco Qual Supervis & Test Ctr, Zhengzhou 450001, Peoples R China
推荐引用方式
GB/T 7714		 Zhang, Sen,Zhang, Jingni,Cheng, Wanyan,et al. Combined cell death of co-exposure to aldehyde mixtures on human bronchial epithelial BEAS-2B cells: Molecular insights into the joint action[J]. CHEMOSPHERE,2020,244.
APA Zhang, Sen.,Zhang, Jingni.,Cheng, Wanyan.,Chen, Huan.,Wang, An.,...&Hu, Qingyuan.(2020).Combined cell death of co-exposure to aldehyde mixtures on human bronchial epithelial BEAS-2B cells: Molecular insights into the joint action.CHEMOSPHERE,244.
MLA Zhang, Sen,et al."Combined cell death of co-exposure to aldehyde mixtures on human bronchial epithelial BEAS-2B cells: Molecular insights into the joint action".CHEMOSPHERE 244(2020).

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来源：合肥物质科学研究院

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