<p>Cadmium (Cd) is a toxic heavy metal known to induce oxidative stress and disrupt physiological functions during development. In this study, we investigated the protective effects of glutathione (GSH) against cadmium chloride (CdCl₂)-induced toxicity in zebrafish embryos. Our results showed that exposure to CdCl₂ increased cell death in the head region of zebrafish at 72&#xa0;h post-fertilization (hpf) in a dose-dependent manner, with a significant elevation in the levels of reactive oxygen species (ROS) at concentrations of ≥ 1&#xa0;µM at 48 hpf. Co-treatment with GSH at a concentration of 100&#xa0;µM effectively suppressed both cell death and ROS generation. CdCl₂ exposure also caused a significant reduction in heart rate at 72 hpf, which was rescued by GSH at 1&#xa0;µM CdCl₂ but not at higher concentrations. Although GSH failed to restore 5-hydroxytryptamine (5-HT/serotonin) levels in embryos treated with 10&#xa0;µM CdCl₂, the Cd-induced suppression of heart rate was reversed by the serotonergic (5-HTergic) modulators quipazine and fluoxetine, suggesting the involvement of the 5-HT system in Cd-induced cardiotoxicity. Behavioral assessments further revealed that CdCl₂ impaired tactile response and altered swimming activity, both of which were ameliorated by the addition of GSH. Together, these findings demonstrate that GSH attenuates Cd-induced neurotoxicity, cardiotoxicity, and behavioral impairments in zebrafish, highlighting its potential as a protective agent against heavy metal toxicity during early development.</p>