Metal coordination chemistry underlying environmentally driven neurological damage
Busurat Adenike Mudashiru1*, Roqeebat Abiodun Mudashiru2
Abstract
Neurological damage associated with environmental metal exposure represents a convergence of coordination chemistry, redox biology, and neurophysiology. Metals such as lead, mercury, manganese, arsenic, iron, copper, nickel, aluminum, and cadmium possess distinct coordination behaviors that dictate their biological fate, cellular distribution, and neurotoxic potential. Unlike organic neurotoxicants, metals exert toxicity not through covalent modification but through coordination interactions with proteins, nucleic acids, membranes, and small-molecule ligands. These interactions alter enzyme activity, disrupt neurotransmission, destabilize metal homeostasis, and induce oxidative and nitrosative stress. In the nervous system, where redox balance, metal cofactors, and synaptic signaling are tightly regulated, even subtle perturbations in coordination chemistry can propagate into long-term neurodegeneration, cognitive impairment, and developmental deficits. This review synthesizes journal evidence linking environmental metal exposure to neurological damage through coordination-driven mechanisms, emphasizing metal speciation, ligand competition, redox cycling, protein misfolding, mitochondrial dysfunction, and neuroinflammation. Particular attention is given to how coordination geometry, oxidation state, and ligand environment govern blood–brain barrier transport, intracellular localization, and persistence of metals in neural tissue. The review concludes by identifying emerging analytical approaches and regulatory implications, arguing that neurological risk assessment must incorporate coordination chemistry rather than relying solely on total metal concentration.
Keywords:
Coordination chemistry; Neurotoxicity; Metal speciation; Blood–brain barrier; Oxidative stress; Synaptic dysfunction; Protein misfolding; Mitochondrial damage; Neuroinflammation; Environmental exposure
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