What Makes a Natural Clay Antibacterial?

Natural clays have been used in ancient and modern medicine, but the mechanism(s) that make certain clays lethal against bacterial pathogens has not been identified. We have compared the depositional environments, mineralogies, and chemistries of clays that exhibit antibacterial effects on a broad s...

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Published inEnvironmental science & technology Vol. 45; no. 8; pp. 3768 - 3773
Main Authors Williams, Lynda B, Metge, David W, Eberl, Dennis D, Harvey, Ronald W, Turner, Amanda G, Prapaipong, Panjai, Poret-Peterson, Amisha T
Format Journal Article
LanguageEnglish
Published Washington, DC American Chemical Society 15.04.2011
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Abstract Natural clays have been used in ancient and modern medicine, but the mechanism(s) that make certain clays lethal against bacterial pathogens has not been identified. We have compared the depositional environments, mineralogies, and chemistries of clays that exhibit antibacterial effects on a broad spectrum of human pathogens including antibiotic resistant strains. Natural antibacterial clays contain nanoscale (<200 nm), illite-smectite and reduced iron phases. The role of clay minerals in the bactericidal process is to buffer the aqueous pH and oxidation state to conditions that promote Fe2+ solubility. Chemical analyses of E. coli killed by aqueous leachates of an antibacterial clay show that intracellular concentrations of Fe and P are elevated relative to controls. Phosphorus uptake by the cells supports a regulatory role of polyphosphate or phospholipids in controlling Fe2+. Fenton reaction products can degrade critical cell components, but we deduce that extracellular processes do not cause cell death. Rather, Fe2+ overwhelms outer membrane regulatory proteins and is oxidized when it enters the cell, precipitating Fe3+ and producing lethal hydroxyl radicals.
AbstractList Natural clays have been used in ancient and modern medicine, but the mechanism(s) that make certain clays lethal against bacterial pathogens has not been identified. We have compared the depositional environments, mineralogies, and chemistries of clays that exhibit antibacterial effects on a broad spectrum of human pathogens including antibiotic resistant strains. Natural antibacterial clays contain nanoscale (<200 nm), illite-smectite and reduced iron phases. The role of clay minerals in the bactericidal process is to buffer the aqueous pH and oxidation state to conditions that promote Fe 2+ solubility. Chemical analyses of E. coli killed by aqueous leachates of an antibacterial clay show that intracellular concentrations of Fe and P are elevated relative to controls. Phosphorus uptake by the cells supports a regulatory role of polyphosphate or phospholipids in controlling Fe 2+ . Fenton reaction products can degrade critical cell components, but we deduce that extracellular processes do not cause cell death. Rather, Fe 2+ overwhelms outer membrane regulatory proteins and is oxidized when it enters the cell, precipitating Fe 3+ and producing lethal hydroxyl radicals.
Natural clays have been used in ancient and modern medicine, but the mechanism(s) that make certain clays lethal against bacterial pathogens has not been identified. We have compared the depositional environments, mineralogies, and chemistries of clays that exhibit antibacterial effects on a broad spectrum of human pathogens including antibiotic resistant strains. Natural antibacterial clays contain nanoscale (<200 nm), illite-smectite and reduced iron phases. The role of clay minerals in the bactericidal process is to buffer the aqueous pH and oxidation state to conditions that promote Fe(2+) solubility. Chemical analyses of E. coli killed by aqueous leachates of an antibacterial clay show that intracellular concentrations of Fe and P are elevated relative to controls. Phosphorus uptake by the cells supports a regulatory role of polyphosphate or phospholipids in controlling Fe(2+). Fenton reaction products can degrade critical cell components, but we deduce that extracellular processes do not cause cell death. Rather, Fe(2+) overwhelms outer membrane regulatory proteins and is oxidized when it enters the cell, precipitating Fe(3+) and producing lethal hydroxyl radicals.
Natural clays have been used in ancient and modern medicine, but the mechanism(s) that make certain clays lethal against bacterial pathogens has not been identified. We have compared the depositional environments, mineralogies, and chemistries of clays that exhibit antibacterial effects on a broad spectrum of human pathogens including antibiotic resistant strains. Natural antibacterial clays contain nanoscale (<200 nm), illite-smectite and reduced iron phases. The role of clay minerals in the bactericidal process is to buffer the aqueous pH and oxidation state to conditions that promote Fe2+ solubility. Chemical analyses of E. coli killed by aqueous leachates of an antibacterial clay show that intracellular concentrations of Fe and P are elevated relative to controls. Phosphorus uptake by the cells supports a regulatory role of polyphosphate or phospholipids in controlling Fe2+. Fenton reaction products can degrade critical cell components, but we deduce that extracellular processes do not cause cell death. Rather, Fe2+ overwhelms outer membrane regulatory proteins and is oxidized when it enters the cell, precipitating Fe3+ and producing lethal hydroxyl radicals. [PUBLICATION ABSTRACT]
Natural clays have been used in ancient and modern medicine, but the mechanism(s) that make certain clays lethal against bacterial pathogens has not been identified. We have compared the depositional environments, mineralogies, and chemistries of clays that exhibit antibacterial effects on a broad spectrum of human pathogens including antibiotic resistant strains. Natural antibacterial clays contain nanoscale (<200 nm), illite-smectite and reduced iron phases. The role of clay minerals in the bactericidal process is to buffer the aqueous pH and oxidation state to conditions that promote Fe2+ solubility. Chemical analyses of E. coli killed by aqueous leachates of an antibacterial clay show that intracellular concentrations of Fe and P are elevated relative to controls. Phosphorus uptake by the cells supports a regulatory role of polyphosphate or phospholipids in controlling Fe2+. Fenton reaction products can degrade critical cell components, but we deduce that extracellular processes do not cause cell death. Rather, Fe2+ overwhelms outer membrane regulatory proteins and is oxidized when it enters the cell, precipitating Fe3+ and producing lethal hydroxyl radicals.
Author Prapaipong, Panjai
Harvey, Ronald W
Metge, David W
Poret-Peterson, Amisha T
Williams, Lynda B
Turner, Amanda G
Eberl, Dennis D
AuthorAffiliation Arizona State University
U.S. Geological Survey
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  fullname: Poret-Peterson, Amisha T
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Keywords Clay
Pharmacological activity
Antiseptic
Natural product
Physicochemical properties activity relationship
Antibacterial agent
Biological activity
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Snippet Natural clays have been used in ancient and modern medicine, but the mechanism(s) that make certain clays lethal against bacterial pathogens has not been...
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StartPage 3768
SubjectTerms Aluminum Silicates - chemistry
Aluminum Silicates - toxicity
Anti-Bacterial Agents - analysis
Anti-Bacterial Agents - chemistry
Anti-Bacterial Agents - toxicity
Antibacterial agents
Antibiotics. Antiinfectious agents. Antiparasitic agents
Biological and medical sciences
Cells
Clay
E coli
Ecotoxicology and Human Environmental Health
Environmental science
Escherichia coli - drug effects
Escherichia coli - metabolism
Escherichia coli - ultrastructure
Hydrogen-Ion Concentration
Hydroxyl Radical - chemistry
Iron
Iron - metabolism
Medical sciences
Microscopy, Electron, Transmission
Minerals - analysis
Minerals - chemistry
Minerals - toxicity
Oxidation
Oxidation-Reduction
Pathogens
Pharmacology. Drug treatments
Phosphorus - metabolism
Silicates - analysis
Silicates - chemistry
Silicates - toxicity
Title What Makes a Natural Clay Antibacterial?
URI http://dx.doi.org/10.1021/es1040688
https://www.ncbi.nlm.nih.gov/pubmed/21413758
https://www.proquest.com/docview/866422967/abstract/
https://pubmed.ncbi.nlm.nih.gov/PMC3126108
Volume 45
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