ABSTRACT Arsenic contamination in aquatic ecosystems is a major environmental concern. Selenium (Se) helps mitigate oxidative stress and hence could reduce the toxic effects of arsenic. However, Se can also be toxic at high concentrations. Given that these metalloids commonly co‐occur in the environment, there is a pressing need for further research into their combined effects on aquatic life. To investigate this interplay, zebrafish embryos were exposed to As alone (as arsenite) or in combination with two different chemical forms of Se including As 120 μg/L alone (as arsenite), As 120 μg/L + Se 25 μg/L (as selenite), As 120 μg/L + Se 120 μg/L (as selenite), and As 120 μg/L + Se 2.5 μg/L (as selenomethionine, SeMet) until 4 days postfertilization. There was no significant difference in the survival, hatching, and deformity rate when fish were exposed to both As and Se. Co‐exposure to As and Se significantly affected thigmotaxis and reflexive movement (for all p < 0.05), with 2.5 μg/L Se mitigating As‐induced impairments. While reactive oxygen species (ROS) levels were elevated in larvae exposed to As alone and As + Se 25 μg/L, there were markedly reduced ROS levels in the As + Se 120 μg/L and As + Se 2.5 μg/L treatments, highlighting Se's antioxidant efficacy. A marked suppression of genes related to antioxidant, neurogenesis, dopaminergic, serotonergic, and motor neurons was observed following arsenic exposure. At the same time, co‐treatment with As + Se 25 μg/L partially restored nrf2a expression ( p < 0.05). These findings highlight the potential for naturally co‐occurring Se to modulate As toxicity in aquatic environments, underscoring the importance of considering chemical interactions when assessing ecological risks.
Luo et al. (2026) studied this question.