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Transition metal ions, specifically Zinc (Zn) and Iron (Fe), are indispensable micronutrients that function as essential cofactors for approximately 10% of the human proteome [10, 11]. Iron is central to oxygen transport in hemoglobin and cellular respiration via cytochromes, while Zinc provides structural integrity to zinc finger transcription factors and catalyzes reactions in over 300 enzymes [11, 12]. Dysregulation of these ions—whether through deficiency or toxic accumulation—is a hallmark of various conditions, including iron-deficiency anemia, hereditary hemochromatosis, and neurodegenerative diseases like Alzheimer's, where metal-induced oxidative stress contributes to pathology [9, 16, 23]. In clinical practice, these ions are targeted via chelation therapy to remove excess levels or through supplementation to address deficiencies [4, 23]. Furthermore, many therapeutic agents achieve their effect by binding to the metal centers of metalloenzymes, highlighting the role of these ions as critical focal points for drug action [14, 19].
Chelation (sequestration and excretion), supplementation (restoring physiological levels), and competitive inhibition of absorption or enzyme activity by binding to metal centers.
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