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Lipidomics Atlas Tracks Alterations Associated with Deltamethrin-Induced Developmental Neurotoxicity in Embryonic Zebrafish

文献类型： 外文期刊

作者： Gao, Longhua 1 ; Hao, Jingwen 1 ; Hua, Zhengyi 4 ; Zeng, Changchun 5 ; Li, Jia 2 ; Zeng, Jun 1 ;

作者机构： 1.Jimei Univ, Coll Ocean Food & Biol Engn, Xiamen 361021, Peoples R China

2.Chinese Acad Agr Sci, Tea Res Inst, Key Lab Tea Biol & Resources Utilizat, Minist Agr, Hangzhou 310008, Peoples R China

3.Xiamen Key Lab Marine Funct Food, Xiamen 361021, Peoples R China

4.Xiamen Univ, Sch Life Sci, Xiamen 361102, Peoples R China

5.Shenzhen Longhua Dist Cent Hosp, Dept Med Lab, Shenzhen 518110, Peoples R China

6.Helmholtz Munich, Res Unit Analyt BioGeoChem, D-85764 Neuherberg, Germany

关键词： deltamethrin; lipidomics; zebrafish; developmental neurotoxicity

期刊名称：JOURNAL OF PROTEOME RESEARCH （ 影响因子：3.6； 五年影响因子：4.0 ）

ISSN： 1535-3893

年卷期： 2025 年 24 卷 5 期

页码：

收录情况： SCI

摘要： Deltamethrin (DM) is a widely used pyrethroid pesticide associated with childhood neurodevelopmental disorders. However, the specific impact of DM exposure during distinct early life stages remains unclear. Here, zebrafish embryos were exposed to DM at different stages: before (10-16 hpf), at the onset of (16-24 hpf), at the peak of (24-36 hpf) hypothalamic neurogenesis, and continuously from 10 to 120 hpf (subchronic exposure), using different dosages (1, 100, and 250 nM). Exposure to middle/high-dose DM at 24-36 and 10-120 hpf significantly reduced zebrafish locomotor activities and increased apoptotic cells in the spinal cord. As a pivotal factor in central nervous system disorder progression, altered lipid metabolism was investigated using nontargeted lipidomic analysis. DM exposure at 10-16 and 24-36 hpf led to the most significant lipidome reprogramming. Despite exhibiting a dose-dependent trend, even low-dose DM changed the lipidome. Cer 40:2;2 and PG 44:12 showed potential in identifying DM exposure effects. Significant changes in sphingolipid, cardiolipin, phosphatidylglycerol, and glycerolipid pathways were linked to DM-induced developmental neurotoxicity, indicating impaired membrane function, mitochondrial damage, and disrupted energy metabolism. Our study sheds new light on assessing early neurodevelopmental disturbances and identifying intervention targets, emphasizing sensitivity to DM during the critical early phase of neurodevelopment.

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