Imidacloprid affects human cells through mitochondrial dysfunction and oxidative stress
文献类型：期刊论文
| 作者 | Wei, Fenghua2,3; Cheng, Fei1,2; Li, Huizhen2; You, Jing2 |
| 刊名 | SCIENCE OF THE TOTAL ENVIRONMENT
 |
| 出版日期 | 2024-11-15 |
| 卷号 | 951页码:10 |
| 关键词 | Neonicotinoids insecticides Imidacloprid Mitochondrial dysfunction Human health threshold SH-SY5Y cells |
| ISSN号 | 0048-9697 |
| DOI | 10.1016/j.scitotenv.2024.175422 |
| 英文摘要 | Given their relatively low persistence and mammalian toxicity, neonicotinoid pesticides have been extensively used worldwide and are omnipresent in the environment. Recent studies have shown that neonicotinoids may pose adverse effects on non-target organisms other than the known neurotoxicity, raising emerging concerns that these insecticides might pose human health risk through additional toxicity pathways. In the present study, the mitochondria function, oxidative stress, DNA damages, and genes transcription levels were examined in the human neuroblastoma SH-SY5Y cells after 48-h exposure to imidacloprid at concentrations from 0.05 to 200 mu mol/L. Results showed that imidacloprid induced mitochondrial dysfunction with the degradation of adenosine triphosphate (ATP) and mitochondrial membrane potential (MMP) levels. In addition, imidacloprid caused oxidative stress by stimulating the generation of reactive oxygen species (ROS) and hydrogen peroxide (H2O2) via the disruption of calcium ion level and mitochondrial function. Ultimately, the oxidative stress continued to produce DNA damage and apoptosis in SH-SY5Y cells at imidacloprid concentrations above 47.6 mu mol/L. Among the evaluated endpoints, ATP was the most sensitive, with a median activity concentration of 0.74 mu mol/L. The 5 % hazard concentration of imidacloprid was estimated to be 0.69 mu mol/L, which can be used as a threshold for human health risk assessment for imidacloprid. Collectively, our results provide an important support for further research on potential toxicity of neonicotinoids related to mitochondrial toxicity in humans. |
| WOS研究方向 | Environmental Sciences & Ecology |
| 语种 | 英语 |
| WOS记录号 | WOS:001295776500001 |
| 源URL | [http://ir.gig.ac.cn/handle/344008/80413]  |
| 专题 | 有机地球化学国家重点实验室 |
| 通讯作者 | You, Jing |
| 作者单位 | 1.Chinese Acad Sci, Guangzhou Inst Geochem, State Key Lab Organ Geochem, Guangzhou 510640, Peoples R China 2.Jinan Univ, Coll Environm & Climate, Guangdong Prov Key Lab Environm Pollut & Hlth, Guangzhou 510632, Peoples R China 3.Jiaying Univ, Sch Chem & Environm, Meizhou 514015, Peoples R China |
| 推荐引用方式 GB/T 7714 | Wei, Fenghua,Cheng, Fei,Li, Huizhen,et al. Imidacloprid affects human cells through mitochondrial dysfunction and oxidative stress[J]. SCIENCE OF THE TOTAL ENVIRONMENT,2024,951:10. |
| APA | Wei, Fenghua,Cheng, Fei,Li, Huizhen,&You, Jing.(2024).Imidacloprid affects human cells through mitochondrial dysfunction and oxidative stress.SCIENCE OF THE TOTAL ENVIRONMENT,951,10. |
| MLA | Wei, Fenghua,et al."Imidacloprid affects human cells through mitochondrial dysfunction and oxidative stress".SCIENCE OF THE TOTAL ENVIRONMENT 951(2024):10. |
入库方式： OAI收割
来源：广州地球化学研究所
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