Evaluation of Maghemite Nanoparticles-Induced Developmental Toxicity and Oxidative Stress in Zebrafish Embryos/Larvae

Maghemite nanoparticles ([Formula: see text] NPs) have a wide array of applications in various industries including biomedical field. There is an absence of legislation globally for the regulation of the production, use, and disposal of such NPs as they are eventually dumped into the environment where these NPs might affect the living systems. This study evaluates the effect of the [Formula: see text] NP-induced developmental toxicity in zebrafish embryos/larvae. The commercially available Fe₂O₃ NPs were purchased, and zebrafish embryos toxicity test was done by exposing embryos to various concentrations of [Formula: see text] NPs at 1 hpf and analyzed at 96 hpf. Based on the LC₅₀ value (60.17 ppm), the sub-lethal concentrations of 40 and 60 ppm were used for further experiments. Hatching, lethality, developmental malformations, and heartbeat rate were measured in the control and treated embryos/larvae. The ionic Fe content in the media, and the larvae was quantified using ICP-MS and AAS. The biomolecular alterations in the control and treated groups were analyzed using FT-IR. The Fe ions present in the larvae were visualized using SEM-EDXS. In situ detection of AChE and apoptotic bodies was done using staining techniques. Biochemical markers (total protein content, AChE, and Na⁺ K⁺-ATPase) along with oxidants and antioxidants were assessed. A significant decrease in the heartbeat rate and hatching delay was observed in the treated groups affecting the developmental processes. Teratogenic analysis showed increased developmental deformity incidence in treated groups in a dose-dependent manner. The accumulation of Fe was evidenced from the ICP-MS, AAS, and SEM-EDXS. Alterations in AChE and Na⁺ K⁺-ATPase activity were observed along with an increment in the oxidants level with a concomitant decrease in antioxidant enzymes. These results show [Formula: see text] NP exposure leads to developmental malformation and results in the alteration of redox homeostasis.