Developmental toxicity and neurobehavioral effects of sodium selenite and selenium nanoparticles on zebrafish embryos

Selenium, a trace mineral, is essential for several physiological processes in humans and animals. It is an antioxidant vital for the immunological response, DNA synthesis, thyroid hormone metabolism, and antioxidant defense enzymes. Zebrafish embryos and larvae were exposed to different concentrations of sodium selenite (SodSe) and selenium nanoparticles (SeNs) at various developmental stages. The study evaluated the impact of SodSe and SeNs on larvae survival, hatching rate, and morphological abnormalities. Also, acridine orange staining was used to analyze the apoptotic cell death, and behavioral tests were conducted to assess anxiety-like behaviors. The results showed that both SodSe and SeNs influence the development and neurobehavior of zebrafish larvae in a concentration-dependent manner. SodSe at high concentration causes low survival rates, delayed hatching, and increased morphological defects in zebrafish larvae. In addition, exposure to SodSe resulted in elevated apoptosis in different larval tissues. Zebrafish larvae treated with SodSe and SeNs exhibited anxiety-like behaviour, increased thigmotaxis, less exploratory behaviour, and less swimming patterns. The nerve conductions and stimuli responses evaluated through acetylcholine esterase (AChE) and cortisol assays, revealed a decrease in the activity in a dose-dependent manner of SodSe and SeNs. Interestingly, the effects of SeNs were lower even at higher concentrations when compared with SodSe at lower concentrations on zebrafish embryos. This shows that SeNs synthesized through biological methods may be less toxic and may have lower effect on the development and neurobehavior of zebrafish larvae. Thus, our study confirms the cytotoxic and neurobehavioral effects of SodSe and suggests the use of SeNs at lower concentration to provide insights into better understanding of developmental stages and metabolic pathways in zebrafish larvae.