Mercury (Hg) is a pervasive environmental contaminant with potent neurotoxic, teratogenic, and systemic effects. Both inorganic (HgCl2) and organic (MeHgCl) forms disrupt development, inducing oxidative stress, mitochondrial dysfunction, altered neurotransmission, and gene expression changes. Zebrafish (Danio rerio) serve as a powerful model for mercury research due to their genetic and physiological similarities to humans, rapid external development, transparent embryos, and well‑characterized behavior. Mercury exposure in zebrafish leads to developmental abnormalities, including delayed hatching, morphological malformations, impaired muscle and skeletal formation, and disrupted pigmentation. Neurobehavioral effects include altered locomotor activity, anxiety‑like behavior, deficits in learning and memory, and impaired social interactions, reflecting disruptions in dopaminergic, serotonergic, and glutamatergic pathways. Physiologically, mercury induces oxidative stress, compromises cardiovascular and immune function, disrupts endocrine regulation, and reduces reproductive capacity. These effects underscore mercury’s multifaceted toxicity and highlight zebrafish as a translational model for studying mechanisms of neurobehavioral and systemic damage. Integrating behavioral, developmental, and physiological endpoints provides a comprehensive framework for understanding mercury toxicity and informing environmental and public health strategies. Thus, mercury exposure can also provide insight into potential dental toxicity, including impaired mineralization, craniofacial malformations, and disruption of odontogenesis pathways.