Exposure to propylparaben induces craniofacial bone developmental toxicity through ROS-induced oxidative stress and apoptosis in zebrafish (Danio rerio) embryos.

Propylparaben (PrP) is an extensively utilized antimicrobial preservative in food industry, cosmetics, personal care products, and pharmaceuticals. Nevertheless, the toxicological effects of PrP on animals are still not well characterized. In this study, zebrafish embryos and larvae were exposed to PrP at concentrations of 5, 7.5, and 10 μM from 10 h post-fertilization (hpf) to 4 days post-fertilization (dpf), reflecting international safety standards. PrP exposure induced severe craniofacial cartilage deformities in larvae at 4 dpf, concomitant with a significant elevation in oxidative stress. Biochemical analyses confirmed markedly increased the activities of the antioxidant superoxide dismutase (SOD) and enzymes catalase (CAT), alongside elevated malondialdehyde (MDA) levels, indicating lipid peroxidation. RT-qPCR revealed downregulated expression of key chondrogenic marker genes (col2a1a, sox9a, sox9b). Additionally, morphological alterations in maxillofacial chondrocytes were observed, driven by significantly enhanced apoptosis without significant inhibition of proliferation. Critically, cotreatment with the antioxidant astaxanthin (AST) partially rescued craniofacial cartilage development. These findings demonstrate that PrP-induced oxidative stress promotes chondrocyte apoptosis, leading to craniofacial malformations in zebrafish embryos.