Hyperoside exposure impairs cardiac development in zebrafish embryos: Evidence from phenotyping, transcriptomics, and antioxidant rescue.

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.