Triclopyr disrupts oxidative balance, energy metabolism, and behaviour in zebrafish (Danio rerio) embryo.

Triclopyr is a widely used auxin-mimicking herbicide frequently detected in aquatic environments. Despite its widespread use, information regarding its sublethal effects during vertebrate development remains limited. This study investigated the effects of developmental exposure to triclopyr on oxidative balance, energy metabolism, cardiac function, and behaviour using zebrafish (Danio rerio) embryos and larvae as a model. Embryos were exposed from fertilization to 120 h post-fertilization to 0.125, 0.470, 1.768, 6.648, and 25 mg L-1 triclopyr. Exposure induced bradycardia at all tested concentrations after 48 h of development, indicating early cardiophysiological impairment. In larvae, triclopyr stimulated antioxidant responses at 6.648 mg L-1 and altered metabolic pathways associated with cellular stress, including increased anaerobic metabolism at 0.125 and 1.768 mg L-1. These biochemical changes were accompanied by increased energetic demand and reduced cellular energy allocation at most tested concentrations, suggesting disruption of energy homeostasis during development. Furthermore, larvae exposed to 1.768 and 6.648 mg L-1 exhibited reduced locomotor performance and increased inactivity, demonstrating that molecular and physiological disturbances translated into organism-level functional effects. Together, these findings indicate that triclopyr can impair multiple biological processes during early zebrafish development, linking oxidative imbalance and metabolic disruption to adverse physiological and behavioural outcomes. The results contribute to a better understanding of the mechanisms underlying triclopyr toxicity and highlight the importance of considering sublethal endpoints when evaluating the ecological risks of herbicide exposure in aquatic organisms.