详细信息

Parental exposure to Cypermethrin causes intergenerational toxicity in zebrafish offspring  ( SCI-EXPANDED收录 EI收录)  

文献类型:期刊文献

英文题名:Parental exposure to Cypermethrin causes intergenerational toxicity in zebrafish offspring

作者:Han, Shuang[2,3];Liu, Xi[3];Liu, Yixiang[1];Lu, Jian[1,3]

机构:[1]Yunnan Agr Univ, State Key Lab Conservat & Utilizat Bioresources Yu, Kunming, Peoples R China;[2]Chinese Acad Sci, Shanghai Inst Nutr & Hlth, Morphol & Spatial Multiomics Technol Platform, Yueyang Rd 320, Shanghai 200031, Peoples R China;[3]East China Univ Sci & Technol, Sch Pharm, Shanghai Key Lab Chem Biol, Shanghai 200237, Peoples R China

年份:2024

卷号:935

外文期刊名:SCIENCE OF THE TOTAL ENVIRONMENT

收录:;EI(收录号:20242116138352);WOS:【SCI-EXPANDED(收录号:WOS:001246330200001)】;

基金:This work was financially sponsored by Yunnan Xingdian Talent Support Program and Scientific Research Fund Project of Yunnan Pro- vincial Department of Education (NO. 2024J0427) , Yunnan Provincial Science and Technology Department (No. 202401BD070001-067) .

语种:英文

外文关键词:Cypermethrin; Development toxicity; Zebrafish; Intergenerational transmission; Swim bladder

摘要:Cypermethrin (CYP), a synthetic pyrethroid pesticide, has been detected in agriculture and aquaculture. However, there is limited knowledge about the transgenerational impacts. This study aimed to investigate the developmental toxicity of CYP on F1 larvae offspring of adult zebrafish exposed to various CYP concentrations (5, 10, and 20 mu g/L) for 28 days. The results indicated that CYP accumulated in parental zebrafish, and CYP was below the limit of quantification in offspring. Paternal exposure impacted the hatching rate and heart rate of the F1 generation. Furthermore, CYP significantly impacted the development of swim bladders in progeny and dysregulated the genes relevant to swim bladder development. The neutrophil migrated to the swim bladder. The mRNA levels of the inflammatory factors were also significantly elevated. According to network toxicology, PI3AKT may be the signaling pathway for CYP-influenced bladder development. Subsequent molecular docking and Western blot analysis showed CYP affected the PI3-AKT signaling pathway. Notably, MK-2206, a specific Akt inhibitor, rescued the CYP-induced damage of swim bladder development in offspring. The present study highlights the potential risks of CYP on the development of offspring and lasting impact in aquatic environments.

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