[特邀报告]新型烟碱类农药人群暴露生物标志物的识别

新型烟碱类农药人群暴露生物标志物的识别
编号:4321 稿件编号:3020 访问权限:仅限参会人 更新:2024-04-15 20:45:32 浏览:468次 特邀报告

报告开始:2024年05月18日 14:35 (Asia/Shanghai)

报告时间:15min

所在会议:[S5] 主题5、环境科学 » [S5-1] 主题5、环境科学 专题5.6、专题5.13、专题5.7(18日下午,307)

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摘要
As the mitochondrial DNA copy number (mtDNAcn) had been reported to be a biomarker for mtDNA damage in honeybees when exposed to sublethal neonicotinoids, the feasibility of human mitochondria as a predictor upon neonicotinoid exposure remains elusive. This study investigated the association between the urinary neonicotinoid and the relative mtDNAcn (RmtDNAcn) of oral epithelial cells collected in a cross-sectional study with repeated measurements over six weeks. The molecular mechanism underlying neonicotinoid-caused mitochondrial damage was also examined by in vitro assay. Herein, the average integrated urinary neonicotinoids (IMIRPF) concentration ranged from 8.01 to 13.70 μg/L (specific gravity-adjusted) during the sampling period. Concomitantly with an increase in urinary IMIRPF, RmtDNAcn significantly increased from 1.20 (Low group) to 1.93 (High group), indicating potential dose-dependent mitochondrial damage. Furthermore, the linear regression analysis confirmed the significant correlation between IMIRPF and RmtDNAcn. Results from in vitro assays demonstrated that neonicotinoid exposure led to the inhibition of genes encoding mitochondrial oxidative phosphorylation (OXPHOS) complex I and III (e.g., ND2, ND6, CytB, and CYC1), accompanied by increased reactive oxygen species (ROS) production in SH-SY5Y cells. Conjointly, neonicotinoid exposure led to mitochondrial dysfunction and the resulting increase in RmtDNAcn, which may serve as a plausible biomarker for humans.
 
关键字
Neonicotinoids,Mitochondrial DNA,Oral epithelial cells,Urine,Biomarker
报告人
张全
教授 浙江工业大学

稿件作者
张全 浙江工业大学
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