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Mercury(II) ion (Hg2+), also known as the mercuric ion, is a highly toxic divalent cation and a prevalent form of inorganic mercury exposure [1, 2]. It is not a physiological component of the human body but acts as a potent environmental toxin and xenobiotic [2]. The primary mechanism of Hg2+ toxicity involves its exceptionally high affinity for sulfhydryl (-SH) groups on cysteine residues, leading to the inactivation of various enzymes, structural proteins, and antioxidants like glutathione [2, 3]. This molecular disruption results in severe clinical manifestations, most notably nephrotoxicity, characterized by acute tubular necrosis, and neurotoxicity [2, 4]. While not a therapeutic target in the traditional sense, Hg2+ is the focus of chelation therapy, where drugs such as Succimer (DMSA) and Dimercaprol (BAL) are administered to bind the ion and promote its clearance from the body [2, 5].
Chelation therapy involves the administration of ligands containing sulfhydryl groups that compete with endogenous proteins for the mercury(II) ion, forming stable, non-toxic, and water-soluble complexes that are excreted via the renal or biliary routes [2, 5].
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