Haloxyfop-P-methyl induces immunotoxicity and glucose metabolism disorders and affects the Nrf2/ARE pathway mediated antioxidant system in Chiromantes dehaani
文献类型： 外文期刊
作者： Xu, Wenyue 1 ; Yang, Ying 1 ; Tian, Jiangtao 1 ; Du, Xinglin 1 ; Ye, Yucong 1 ; Liu, Zhiquan 2 ; Li, Yiming 3 ; Zhao, Yunlong 1 ;
作者机构： 1.East China Normal Univ, Sch Life Sci, Shanghai 200241, Peoples R China
2.Hangzhou Normal Univ, Sch Engn, Hangzhou 311121, Zhejiang, Peoples R China
3.Chinese Acad Fisheries Sci, Fishery Machinery & Instrument Res Inst, Shanghai 200092, Peoples R China
4.East China Normal Univ, State Key Lab Estuarine & Coastal Res, Shanghai 200241, Peoples R China
5.East China Normal Univ, Sch Life Sci, 500 Dongchuan Rd, Shanghai 200241, Peoples R China
关键词： Haloxyfop-P-methyl; Growth performance; Glucose metabolism; Immunity; Antioxidant system
期刊名称：ENVIRONMENTAL POLLUTION （ 影响因子：8.9； 五年影响因子：9.5 ）
ISSN： 0269-7491
年卷期： 2023 年 335 卷
页码：
收录情况： SCI
摘要： Haloxyfop-P-methyl is used extensively in agricultural production, and its metabolites in soil have potentially toxic effects on aquatic ecosystems. In this study, we explored the toxicity of haloxyfop-P-methyl on Chiromantes dehaani. The results of the 21-day toxicity test showed that haloxyfop-P-methyl decreased the weight gain (WG), specific growth rate (SGR) and hepatosomatic index (HSI). In glucose metabolism, haloxyfop-P-methyl reduced pyruvate, lactate, lactate dehydrogenase and succinate dehydrogenase, but enhanced glucose-6-phosphate de-hydrogenase and hexokinase. Furthermore, expression of glucose metabolism-related genes was upregulated. We cloned the full-length CdG6PDH gene, which contains a 1587 bp ORF that encoded a 528 amino acid polypeptide. In antioxidant system, haloxyfop-P-methyl increased glutathione, thioredoxin reductase and thioredoxin peroxidase activities and activated the Nrf2/ARE pathway through upregulation of ERK, JNK, PKC and Nrf2. In immunity, low concentrations haloxyfop-P-methyl, or short-term exposure, upregulated the expression of immune-related genes and enhanced immune-related enzymes activity, while high concentrations or long-term exposure inhibited immune function. In summary, haloxyfop-P-methyl inhibited the growth performance, disrupted glucose metabolism, activated the antioxidant system, and led to immunotoxicity. The results deepen our understanding of the toxicity mechanism of haloxyfop-P-methyl and provide basic biological data for the comprehensive assessment of the risk of haloxyfop-P-methyl to the environment and humans.
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