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Acetaldehyde induces similar cytotoxic and genotoxic risks in BEAS-2B cells and HHSteCs: involvement of differential regulation of MAPK/ERK and PI3K/AKT pathways

文献类型：期刊论文

作者Zhang, Jingni1,2,3,4,5,6; Wang, Hongjuan1,2,3,4; Chen, Huan1,2,3,4; Liu, Yong5,6; Wang, An5,6; Hou, Hongwei1,2,3,4; Hu, Qingyuan1,2,3,4,6
刊名ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
出版日期2023-07-01
卷号30
ISSN号0944-1344
关键词Acetaldehyde Cytotoxicity Genotoxicity BEAS-2B cells HHSteCs MAPK/ERK PI3K/AKT
DOI10.1007/s11356-023-27508-x
通讯作者Hu, Qingyuan(huqy1965@163.com)
英文摘要Long-term use of alcohol and cigarettes is associated with millions of deaths each year, directly or indirectly. The carcinogen acetaldehyde is both a metabolite of alcohol and the most abundant carbonyl compound in cigarette smoke, and co-exposure of them is usual and primarily leads to liver and lung injury, respectively. However, few studies have explored the synchronic risk of acetaldehyde on the liver and lung. Here, we investigated the toxic effects and related mechanisms of acetaldehyde based on normal hepatocytes and lung cells. The results showed that acetaldehyde caused significant dose- dependent increases of cytotoxicity, ROS level, DNA adduct level, DNA single/double-strand breakage, and chromosomal damage in BEAS-2B cells and HHSteCs, with similar effects at the same doses. The gene and protein expression and phosphorylation of p38MAPK, ERK, PI3K, and AKT, key proteins of MAPK/ERK and PI3K/AKT pathways regulating cell survival and tumorigenesis, were significantly upregulated on BEAS-2B cells, while only protein expression and phosphorylation of ERK were upregulated significantly, the other three decreased in HHSteCs. When either the inhibitor of the four key proteins was co-treated with acetaldehyde, cell viabilities were almost unchanged in BEAS-2B cells and HHSteCs. Thus, acetaldehyde could synchronically induce similar toxic effects in BEAS-2B cells and HHSteCs, and MAPK/ERK and PI3K/AKT pathways seem to be involved in different regulatory mechanisms.
WOS关键词ENDOGENOUS ALDEHYDES ; ALCOHOL-CONSUMPTION ; DNA-ADDUCTS ; ERK ; ACTIVATION ; APOPTOSIS ; AKT ; NICOTINE ; RECEPTOR ; SMOKING
资助项目Key Laboratory of Tobacco Biological Effects[110202102011]
WOS研究方向Environmental Sciences & Ecology
语种英语
出版者SPRINGER HEIDELBERG
WOS记录号WOS:001061180900009
资助机构Key Laboratory of Tobacco Biological Effects
源URL[http://ir.hfcas.ac.cn:8080/handle/334002/133324]  
专题中国科学院合肥物质科学研究院
通讯作者Hu, Qingyuan
作者单位1.Key Labortory Tobacco Biol Effects & Biosynth, Beijing 102200, Peoples R China
2.Beijing Life Sci Acad, Beijing 102200, Peoples R China
3.Key Lab Tobacco Biol Effects, Zhengzhou 450001, Peoples R China
4.China Natl Tobacco Qual Supervis & Test Ctr, Zhengzhou 450001, Peoples R China
5.Chinese Acad Sci, Hefei Inst Phys Sci, Anhui Inst Opt & Fine Mech, Hefei 230031, Peoples R China
6.Univ Sci & Technol China, Hefei 230026, Peoples R China
推荐引用方式
GB/T 7714		 Zhang, Jingni,Wang, Hongjuan,Chen, Huan,et al. Acetaldehyde induces similar cytotoxic and genotoxic risks in BEAS-2B cells and HHSteCs: involvement of differential regulation of MAPK/ERK and PI3K/AKT pathways[J]. ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH,2023,30.
APA Zhang, Jingni.,Wang, Hongjuan.,Chen, Huan.,Liu, Yong.,Wang, An.,...&Hu, Qingyuan.(2023).Acetaldehyde induces similar cytotoxic and genotoxic risks in BEAS-2B cells and HHSteCs: involvement of differential regulation of MAPK/ERK and PI3K/AKT pathways.ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH,30.
MLA Zhang, Jingni,et al."Acetaldehyde induces similar cytotoxic and genotoxic risks in BEAS-2B cells and HHSteCs: involvement of differential regulation of MAPK/ERK and PI3K/AKT pathways".ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH 30(2023).

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来源：合肥物质科学研究院

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