Semicarbazide conferred developmental toxicity in Oryzias melastigma embryos by oxidative stress and energy metabolism disorder.

The residual antibiotics in aquatic animals present potential risk to ecological environment and food safety. Here, we uncover the biochemical reaction and molecular mechanisms in marine medaka embryos exposed to semicarbazide (SEM) at environmental relevant concentrations (10, 50 and 100 μg/L) for 14 days then followed by 7 days clean water recovery period. The decreased levels total superoxide dismutase (T-SOD) and catalase (CAT), and increased levels in malondialdehyde (MDA) content suggesting SEM induced severe oxidative stress and excessive reactive oxygen species (ROS). These effects further contributed to morphological changes and cardiac dysfunction. Meanwhile, oxidative stress activated genes associated with inflammatory responses (tlr1, cyp1a1, ahr, il-1β), implying potential suppression of innate immune functions. Furthermore, elevated activities of pyruvate kinase (PK), hexokinase (HK), and lactate dehydrogenase (LDH), along with decreased succinate dehydrogenase (SDH) activity, indicated SEM activate glycolysis pathway and disrupt Tricarboxylic Acid cycle (TCA) cycle leading to mitochondrial function and energy metabolism imbalance. Notably, these adverse effects cannot be completely eliminated after the short recovery period, implying a potential long-term toxicity of SEM. This study provides new insights into the toxicity effect SEM on the early developmental of marine organisms, its underlying regulatory mechanisms and implications for SEM risk management.