Has PdCu@GO effect on oxidant/antioxidant balance? Using zebrafish embryos and larvae as a model

Industrial products containing PdCu@GO can gain access to the aquaculture environment, causing dangerous effects on living biota. In this study, the developmental toxicity of zebrafish treated with different concentrations (50, 100, 250, 500 and 1000 μg/L) of PdCu@GO was investigated. The findings showed that PdCu@GO administration decreased the hatchability and survival rate, caused dose-dependent cardiac malformation. Reactive oxygen species (ROS) and apoptosis were also inhibited in a dose-dependent manner, with acetylcholinesterase (AChE) activity affected by nano-Pd exposure. As evidence for oxidative stress, malondialdehyde (MDA) level increased and superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx) activities and glutathione (GSH) level decreased due to the increase in PdCu@GO concentration. Our research, it was determined that the oxidative stress stimulated by the increase in the concentration of PdCu@GO in zebrafish caused apoptosis (Caspase-3) and DNA damage (8-OHdG). Stimulation of ROS, inflammatory cytokines, tumor Necrosis Factor Alfa (TNF-α) and interleukin - 6 (IL-6), which act as signaling molecules to trigger proinflammatory cytokine production, induced zebrafish immunotoxicity. However, it was determined that the increase of ROS induced teratogenicity through the induction of nuclear factor erythroid 2 level (Nrf-2), NF-κB and apoptotic signaling pathways triggered by oxidative stress. Taken together with the research findings, the study contributed to a comprehensive assessment of the toxicological profile of PdCu@GO by investigating the effects on zebrafish embryonic development and potential molecular mechanisms.