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Nickel is a transition metal element that, while essential for certain enzymes in microorganisms and plants, has no confirmed essential biological role in human physiology [1][4]. In humans, it is primarily recognized as a potent allergen and a significant environmental toxicant [2][3]. Exposure to nickel is the leading cause of allergic contact dermatitis and is strongly linked to the development of respiratory tract cancers, including lung and nasal carcinomas, due to its ability to induce oxidative stress and epigenetic alterations [2][5]. From a pharmacological perspective, nickel is not a therapeutic target but rather a substance of toxicological concern [1]. Treatment for nickel exposure involves the use of chelating agents such as disulfiram or EDTA, which bind the metal ions to facilitate their renal excretion [1][5]. Research also explores nickel-dependent enzymes in pathogens, such as urease in Helicobacter pylori, as indirect targets for antimicrobial drug development [4]. Sources: [1] https://pubchem.ncbi.nlm.nih.gov/compound/Nickel [2] https://monographs.iarc.who.int/wp-content/uploads/2018/06/mono100C-10.pdf [3] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047925/ [4] https://pubmed.ncbi.nlm.nih.gov/23575351/ [5] https://www.ncbi.nlm.nih.gov/books/NBK557634/
Chelation of nickel ions to form stable, water-soluble complexes that are subsequently excreted by the kidneys, reducing the body burden of the metal [1][5].
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