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Transition metal ions, including essential elements like copper (Cu) and zinc (Zn) as well as toxic heavy metals like lead (Pb), mercury (Hg), cadmium (Cd), and nickel (Ni), are critical inorganic components that influence human health and disease. Essential metals serve as indispensable cofactors for thousands of enzymes and provide structural integrity to proteins, such as zinc-finger transcription factors and superoxide dismutase [1, 2]. Conversely, non-essential metals like lead and mercury exert toxicity by mimicking essential ions, inducing oxidative stress, and binding to sulfhydryl groups on proteins, leading to systemic organ failure [3]. In a pharmacological context, these ions are the primary targets of chelation therapy, where specific drugs are used to sequester and remove them from the body during instances of acute or chronic poisoning. Because this entry groups multiple distinct chemical species with vastly different biological roles—ranging from essential nutrients to potent environmental toxins—it is categorized as an aggregate rather than a single therapeutic target. Effective management of these ions requires balancing the prevention of deficiency for essential metals with the mitigation of toxicity from environmental exposure [3, 4].
Chelation therapy involves the administration of chelating agents (ligands) that possess electron-donor atoms to form stable, coordinate-covalent bonds with metal ions. This process creates a ring-structured, water-soluble complex that prevents the metal from interacting with cellular components and facilitates its excretion through the kidneys or biliary system [4].
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