ArticleEnvironmental toxicology2026
Exploring Interactive Effects of Arsenic and Selenium Exposure on Larval Zebrafish (Danio rerio).
Article in Environmental toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- N-Acetylcysteine Prevents Arsenic-Induced Apoptosis but Not Supernumerary Motor Neuron Development in Zebrafish Embryos: Assessment of Protein Carbonylation and the p53 Pathway.International journal of molecular sciences · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
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.
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Registered trials
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