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Updated: May 22, 2026
Analysis of Oxidative Stress in Zebrafish Embryos
Published on: July 7, 2014
Hyperoside exposure impairs cardiac development in zebrafish embryos: Evidence from phenotyping, transcriptomics, and
ZhuoShuo Zhou1, Yilin Yang2, Guisen Li3
1Key Laboratory of Microecology-immune Regulatory Network and Related Diseases School of Basic Medicine, Jiamusi University, Jiamusi, Heilongjiang Province 154007, PR China.
None:
Hyperoside, a common flavonoid glycoside, was evaluated for developmental toxicity in zebrafish embryos (6-96 hpf). Hyperoside reduced hatchability and survival (96-h LC50 170.9 μM; LC10 118.3 μM) and caused prominent cardiac defects, including tachycardia, pericardial edema, and atrioventricular malformation, along with altered expression of cardiac markers (nppa, vmhc, sox9b, and gata4). Transcriptomic and phenotypic assays indicated the activation of oxidative stress and apoptosis pathways. Hyperoside increased ROS and MDA, decreased antioxidant enzyme activities (SOD and CAT), and induced apoptosis in the cardiac region (AO staining; baxa/caspase-3/p53 upregulated, bcl2a downregulated). Co-treatment with N-acetyl-L-cysteine (NAC) reduced ROS, attenuated apoptosis, and rescued cardiotoxicity, supporting ROS-driven injury as a key mechanism.
