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References 2025-12-03 18:45:40
Chelation majorpublished
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Removing one metal atom with the right chelator can disable entire virulence systems in multidrug-resistant bacteria, even when all antibiotics fail.
Chelation
Researched by:
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Karen Pendergrass
Karen Pendergrass
Read MoreKaren Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.
Chelation is a biochemical and pharmacological process in which small-molecule chelating agents bind to metal ions with high affinity to sequester, redistribute, or remove metallic elements from biological systems.
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Karen Pendergrass
Read More
Researched by:
-
Karen Pendergrass
Karen Pendergrass
Read More
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Karen Pendergrass
Overview
Chelation is a biochemical and pharmacological process in which small-molecule chelating agents, such as organic compounds, natural metallophores, or synthetic ligands like dimethylglyoxime (DMG), bind to metal ions with high affinity to sequester, redistribute, or remove metallic elements from biological systems.[1] Chelating agents function by surrounding and complexing metal cations through multiple coordinate bonds, thereby reducing the bioavailability and toxicity of toxic metals or redistributing essential metals to maintain physiological homeostasis.[2] For example, dimethylglyoxime is a nickel-specific chelator that exhibits selective binding to nickel and copper ions but not iron, zinc, or selenium, and has demonstrated therapeutic potential in inhibiting amyloid-beta peptide aggregation in Alzheimer’s disease by preventing nickel-enhanced aggregation.[1] Chelation-based interventions operate across multiple biological contexts, from nutritional immunity mechanisms where host proteins like calprotectin sequester bacterial nutrients through metal chelation, to soil remediation applications where glomalin produced by arbuscular mycorrhizal fungi chelates heavy metals to stabilize contaminated environments, representing promising therapeutic strategies for managing metal dyshomeostasis and metal-associated pathologies.[2] [3]
Chelation as Metallome-Targeted Interventions (MTIs)
Chelation represents a sophisticated category of metallome-targeted interventions (MTIs) that employs chelating agents, small molecules or natural compounds with high-affinity metal binding properties, to sequester, redistribute, or remove metal ions from biological systems.[4] Chelation can function therapeutically through multiple mechanisms: reducing bioavailability of toxic metals (e.g., iron or copper sequestration to limit oxidative stress), redistributing metals to normalize dyshomeostasis, or removing accumulated metals in toxic metal overload conditions.[4] Natural metallophores, termed chalkophores, represent biologically-derived chelating compounds that regulate copper bioavailability within microbial communities.[5] The effectiveness of chelation as an MTI depends critically on chemical selectivity for target metals, cellular accessibility, and coordination with other cellular metal homeostatic mechanisms.[4]
Frequently Asked Questions
What is Chelation?
Quick answer: Chelation is a biochemical and pharmacological process in which small-molecule chelating agents, such as organic compounds, natural metallophores, or synthetic ligands like dimethylglyoxime (DMG), bind to metal ions with high affinity to sequester, redistribute, or remove metallic elements from biological systems.[1] Chelating agents function by surrounding and complexing metal cations through multiple coordinate bonds, thereby reducing the bioavailability and toxicity of toxic metals or redistributing essential metals to maintain physiological homeostasis.[2] For example, dimethylglyoxime is a nickel-specific chelator that exhibits selective binding to nickel and copper ions but not iron, zinc, or selenium, and has demonstrated therapeutic potential in inhibiting amyloid-beta peptide aggregation in Alzheimer’s disease by preventing nickel-enhanced aggregation.[1] Chelation-based interventions operate across multiple biological contexts, from nutritional immunity mechanisms where host proteins like calprotectin sequester bacterial nutrients through metal chelation, to soil remediation applications where glomalin produced by arbuscular mycorrhizal fungi chelates heavy metals to stabilize contaminated environments, representing promising therapeutic strategies for managing metal dyshomeostasis and metal-associated pathologies.[2] [3]
What helps treat Chelation?
Quick answer: Chelation represents a sophisticated category of metallome-targeted interventions (MTIs) that employs chelating agents, small molecules or natural compounds with high-affinity metal binding properties, to sequester, redistribute, or remove metal ions from biological systems.[4] Chelation can function therapeutically through multiple mechanisms: reducing bioavailability of toxic metals (e.g., iron or copper sequestration to limit oxidative stress), redistributing metals to normalize dyshomeostasis, or removing accumulated metals in toxic metal overload conditions.[4] Natural metallophores, termed chalkophores, represent biologically-derived chelating compounds that regulate copper bioavailability within microbial communities.[5] The effectiveness of chelation as an MTI depends critically on chemical selectivity for target metals, cellular accessibility, and coordination with other cellular metal homeostatic mechanisms.[4]
Research Feed
Chelation in Metal Intoxication
June 28, 2010
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Metals •
Metals
Heavy metals influence microbial pathogenicity in two ways: they can be toxic to microbes by disrupting cellular functions and inducing oxidative stress, and they can be exploited by pathogens to enhance survival, resist treatment, and evade immunity. Understanding metal–microbe interactions supports better antimicrobial and public health strategies.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
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Current Biomedical Use of Copper Chelation Therapy
February 6, 2020
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Metals •
Metals
Heavy metals influence microbial pathogenicity in two ways: they can be toxic to microbes by disrupting cellular functions and inducing oxidative stress, and they can be exploited by pathogens to enhance survival, resist treatment, and evade immunity. Understanding metal–microbe interactions supports better antimicrobial and public health strategies.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
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The Extracellular Metallometabolome: Metallophores, Metal Ionophores, and Other Chelating Agents as Natural Products
August 28, 2024
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Metals •
Metals
Heavy metals influence microbial pathogenicity in two ways: they can be toxic to microbes by disrupting cellular functions and inducing oxidative stress, and they can be exploited by pathogens to enhance survival, resist treatment, and evade immunity. Understanding metal–microbe interactions supports better antimicrobial and public health strategies.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
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Update History
Dimethylglyoxime (DMG)
Dimethylglyoxime represents a novel therapeutic paradigm that exploits a fundamental metabolic difference between pathogenic bacteria and their mammalian hosts. By selectively depleting bacterial access to nickel, a cofactor essential for multiple pathogenic enzymes but unnecessary for human physiology, DMG offers a theoretically host-sparing antimicrobial approach.
Nutritional Immunity
Nutritional immunity restricts metal access to pathogens, leveraging sequestration, transport, and toxicity to control infections and immunity.
Metals
Heavy metals influence microbial pathogenicity in two ways: they can be toxic to microbes by disrupting cellular functions and inducing oxidative stress, and they can be exploited by pathogens to enhance survival, resist treatment, and evade immunity. Understanding metal–microbe interactions supports better antimicrobial and public health strategies.
Metals
Heavy metals influence microbial pathogenicity in two ways: they can be toxic to microbes by disrupting cellular functions and inducing oxidative stress, and they can be exploited by pathogens to enhance survival, resist treatment, and evade immunity. Understanding metal–microbe interactions supports better antimicrobial and public health strategies.
Metals
Heavy metals influence microbial pathogenicity in two ways: they can be toxic to microbes by disrupting cellular functions and inducing oxidative stress, and they can be exploited by pathogens to enhance survival, resist treatment, and evade immunity. Understanding metal–microbe interactions supports better antimicrobial and public health strategies.
References
- The nickel-chelator dimethylglyoxime inhibits human amyloid beta peptide in vitro aggregation. Benoit SL, Maier RJ. (Sci Rep. 2021;11:6622.)
- Coordinated adaptation of Staphylococcus aureus to calprotectin-dependent metal sequestration. Valeria M. Reyes Ruiz, Jeffrey A. Freiberg et al. (mBio. 2024.)
- The role of glomalin in mitigation of multiple soil degradation problems. A. Singh, Xiai Zhu et al. (Critical Reviews in Environmental Science and Technology. 2020.)
- The Case for Abandoning Therapeutic Chelation of Copper Ions in Alzheimer's Disease. Simon C. Drew. (Frontiers in Neuroscience. 2017.)
- Chalkophores. Grace E. Kenney, Amy C. Rosenzweig. (Annual Review of Biochemistry. 2018.)
Benoit SL, Maier RJ.
The nickel-chelator dimethylglyoxime inhibits human amyloid beta peptide in vitro aggregation.Sci Rep. 2021;11:6622.
Read ReviewValeria M. Reyes Ruiz, Jeffrey A. Freiberg et al.
Coordinated adaptation of Staphylococcus aureus to calprotectin-dependent metal sequestration.mBio. 2024.
A. Singh, Xiai Zhu et al.
The role of glomalin in mitigation of multiple soil degradation problems.Critical Reviews in Environmental Science and Technology. 2020.
Simon C. Drew.
The Case for Abandoning Therapeutic Chelation of Copper Ions in Alzheimer's Disease.Frontiers in Neuroscience. 2017.