Toxic effects of anionic polyacrylamide on the developmental stages of Oryzias melastigma embryos and larvae.

Anionic Polyacrylamide (APAM) is widely used in oil extraction processes, serving as an oil-repellent polymer and constituting a critical component of water-based drilling fluids. The environmental and ecological effects of APAM on fishery resources have attracted significant attention, yet its toxic mechanism in marine fish at early developmental stages remains poorly understood. The potential effects of APAM on marine medaka (Oryzias melastigma) embryos were investigated by exposing them to 0, 120, 240, 480, and 960 mg/L for 18 d. APAM exposure caused developmental toxicity in embryos, leading to reduced heart rates, delayed and decreased hatching, increased mortality and malformations. The activities of superoxide dismutase (SOD) and catalase (CAT) initially increased after 2 d of exposure but decreased after 8 and 18 days of prolonged stress, while malondialdehyde (MDA) concentration increased, causing lipid peroxidation and worsening oxidative damage. After 18 days of APAM exposure, low and medium concentrations increased the expression of cardiovascular genes GATA4 and NKX2.5, while high concentrations decreased NKX2.5, leading to heart defects like elongated hearts and pericardial cysts. Additionally, low concentrations significantly boosted nervous system genes SHHA and SYN2A, enhancing swimming behaviors, whereas high concentrations suppressed these genes, reducing swimming activity. In conclusion, this study demonstrated that APAM exposure causes developmental toxicity, oxidative stress, neurotoxicity, and disrupts early cardiac development in O. melastigma embryos, providing insight into its toxic effects on early marine fish development.