Biological autoxidation I. Decontrolled iron: An ultimate carcinogen and toxicant: An hypothesis
Identifieur interne : 002578 ( Istex/Curation ); précédent : 002577; suivant : 002579Biological autoxidation I. Decontrolled iron: An ultimate carcinogen and toxicant: An hypothesis
Auteurs : S. H. Kon [États-Unis]Source :
- Medical Hypotheses [ 0306-9877 ] ; 1978.
English descriptors
- Teeft :
- Aggregation, Angew chem, Antioxidation, Antioxidation defense, Antioxidation defenses, Antioxidation system, Asbestos, Asbestos bodies, Asbestos body, Asbestos fiber, Autoxidation, Autoxidative crosslinking, Biol chem, Building materials, Carcinogen, Carcinogenesis, Catabolic, Catabolic enzymes, Catabolic insufficiency, Catabolic slowdown, Catalyze autoxidation, Cationic dyes, Cell components, Cell constituents, Chem, Chemical carcinogens, Colloidal, Colloidal particles, Common features, Crosslinking, Defense mechanisms, Degradation, Degraded asbestos, Diffusible pool, Digestion, Dipogenic, Electron microprobe analysis, Electrostatic repulsion, Endogenous, Endogenous lascars, Exogenous, Exogenous agents, Exogenous lascars, Ferric, Ferric hydroxide, Ferritin, Fluctuation, Foreign bodies, Foreign body, Free radicals, Glass fibers, Heinz, Heinz bodies, Hemosiderin, High capacity, Histochem cytochem, Hydrogen ions, Hydrophobic, Hypothetical defense, Initiator, Intracellular, Ionic iron, Iron metabolism, Lascar, Latex particles, Leukocyte, Lipid, Lipid pigments, Liver cirrhosis, Liver lysosomes, Lysosomal, Lysosomal cathepsins, Lysosome, Macromolecular scavenger, Mammalian cells, Metabolic, Metabolic turnover, Metal ions, Moderate rise, Negative charge, Original asbestos fiber, Oxidative, Oxidative crosslinking, Pathol, Phagocytic vacuoles, Phagocytosis, Polymer, Polysilicic acid, Porous body, Positive charge, Preneoplastic carcinogenesis, Primary lascar, Promoter, Protein denaturants, Silicic acid, Small molecules, Sorption, Superoxide, Superoxide dismutase.
Abstract
Abstract: Ionic iron at physiological pH hydrolyzes into insoluble aggregates, which disperse on slight acidification. Uncontrolled ionic iron promotes autoxidation, which crosslinks biomolecules and produces destructive activated oxygen. Defenses against autoxidative crosslinking include: 1. ferritin, the macromolecular scavenger of iron; 2. metabolic turnover, which prevents irreversible crosslinking through early catabolic degradation and replacement; and 3. enzymatic deactivation of oxygen.I am proposing that the anticrosslinking defenses are defeated by transient actions of metabolic perturbations, toxicants, oxidants and “foreign bodies”, which cause oxidative crosslinking of proteins and lipids into irreversible tissue imprint: indigestible bodies containing porous limited-access spaces (LASs). The pores exclude the macromolecular ferritin and the digestive and antiautoxidation enzymes but admit ionic iron which, sheltered from ferritin, accumulates into decontrolled-iron pathogen (DIP). DIP utilizes the energy of ambient pH fluctuations to erupt from the LAS, swamp the available ferritin, poison the surroundings, catalyze autoxidation and crosslink cell components into additional LAS carriers. With time and sufficient promotion by pH fluctuations or metal-complexing agents, DIP and LAS expand. DIP injures through heavy-metal inhibition of life processes and catalysis of autoxidation. Typically, carcinogenic initiators are protein denaturants, cell poisons, “foreign bodies” and autoxidation catalysts. These are DIP-initiating properties, and DIP may be a preneoplastic stage of carcinogenesis. A DIP-model interpretation is given for the growth of asbestos bodies. DIP is an inorganic parasite. It may envelope and attack phagocytized particles.
Url:
DOI: 10.1016/0306-9877(78)90015-4
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Biological autoxidation I. Decontrolled iron: An ultimate carcinogen and toxicant: An hypothesis</title><author><name sortKey="Kon, S H" sort="Kon, S H" uniqKey="Kon S" first="S. H." last="Kon">S. H. Kon</name><affiliation wicri:level="1"><mods:affiliation>The Henry Dazian Department of Chemistry, The Mount Sinai Hospital, New York, New York, 10029, U.S.A.</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>The Henry Dazian Department of Chemistry, The Mount Sinai Hospital, New York, New York, 10029</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:A003605910D73CB021BD0E9B65050263DBF46643</idno><date when="1978" year="1978">1978</date><idno type="doi">10.1016/0306-9877(78)90015-4</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-RLM0HVQH-J/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">002578</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">002578</idno><idno type="wicri:Area/Istex/Curation">002578</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Biological autoxidation I. Decontrolled iron: An ultimate carcinogen and toxicant: An hypothesis</title><author><name sortKey="Kon, S H" sort="Kon, S H" uniqKey="Kon S" first="S. H." last="Kon">S. H. Kon</name><affiliation wicri:level="1"><mods:affiliation>The Henry Dazian Department of Chemistry, The Mount Sinai Hospital, New York, New York, 10029, U.S.A.</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>The Henry Dazian Department of Chemistry, The Mount Sinai Hospital, New York, New York, 10029</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Medical Hypotheses</title><title level="j" type="abbrev">YMEHY</title><idno type="ISSN">0306-9877</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1978">1978</date><biblScope unit="volume">4</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="445">445</biblScope><biblScope unit="page" to="471">471</biblScope></imprint><idno type="ISSN">0306-9877</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0306-9877</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Aggregation</term><term>Angew chem</term><term>Antioxidation</term><term>Antioxidation defense</term><term>Antioxidation defenses</term><term>Antioxidation system</term><term>Asbestos</term><term>Asbestos bodies</term><term>Asbestos body</term><term>Asbestos fiber</term><term>Autoxidation</term><term>Autoxidative crosslinking</term><term>Biol chem</term><term>Building materials</term><term>Carcinogen</term><term>Carcinogenesis</term><term>Catabolic</term><term>Catabolic enzymes</term><term>Catabolic insufficiency</term><term>Catabolic slowdown</term><term>Catalyze autoxidation</term><term>Cationic dyes</term><term>Cell components</term><term>Cell constituents</term><term>Chem</term><term>Chemical carcinogens</term><term>Colloidal</term><term>Colloidal particles</term><term>Common features</term><term>Crosslinking</term><term>Defense mechanisms</term><term>Degradation</term><term>Degraded asbestos</term><term>Diffusible pool</term><term>Digestion</term><term>Dipogenic</term><term>Electron microprobe analysis</term><term>Electrostatic repulsion</term><term>Endogenous</term><term>Endogenous lascars</term><term>Exogenous</term><term>Exogenous agents</term><term>Exogenous lascars</term><term>Ferric</term><term>Ferric hydroxide</term><term>Ferritin</term><term>Fluctuation</term><term>Foreign bodies</term><term>Foreign body</term><term>Free radicals</term><term>Glass fibers</term><term>Heinz</term><term>Heinz bodies</term><term>Hemosiderin</term><term>High capacity</term><term>Histochem cytochem</term><term>Hydrogen ions</term><term>Hydrophobic</term><term>Hypothetical defense</term><term>Initiator</term><term>Intracellular</term><term>Ionic iron</term><term>Iron metabolism</term><term>Lascar</term><term>Latex particles</term><term>Leukocyte</term><term>Lipid</term><term>Lipid pigments</term><term>Liver cirrhosis</term><term>Liver lysosomes</term><term>Lysosomal</term><term>Lysosomal cathepsins</term><term>Lysosome</term><term>Macromolecular scavenger</term><term>Mammalian cells</term><term>Metabolic</term><term>Metabolic turnover</term><term>Metal ions</term><term>Moderate rise</term><term>Negative charge</term><term>Original asbestos fiber</term><term>Oxidative</term><term>Oxidative crosslinking</term><term>Pathol</term><term>Phagocytic vacuoles</term><term>Phagocytosis</term><term>Polymer</term><term>Polysilicic acid</term><term>Porous body</term><term>Positive charge</term><term>Preneoplastic carcinogenesis</term><term>Primary lascar</term><term>Promoter</term><term>Protein denaturants</term><term>Silicic acid</term><term>Small molecules</term><term>Sorption</term><term>Superoxide</term><term>Superoxide dismutase</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Ionic iron at physiological pH hydrolyzes into insoluble aggregates, which disperse on slight acidification. Uncontrolled ionic iron promotes autoxidation, which crosslinks biomolecules and produces destructive activated oxygen. Defenses against autoxidative crosslinking include: 1. ferritin, the macromolecular scavenger of iron; 2. metabolic turnover, which prevents irreversible crosslinking through early catabolic degradation and replacement; and 3. enzymatic deactivation of oxygen.I am proposing that the anticrosslinking defenses are defeated by transient actions of metabolic perturbations, toxicants, oxidants and “foreign bodies”, which cause oxidative crosslinking of proteins and lipids into irreversible tissue imprint: indigestible bodies containing porous limited-access spaces (LASs). The pores exclude the macromolecular ferritin and the digestive and antiautoxidation enzymes but admit ionic iron which, sheltered from ferritin, accumulates into decontrolled-iron pathogen (DIP). DIP utilizes the energy of ambient pH fluctuations to erupt from the LAS, swamp the available ferritin, poison the surroundings, catalyze autoxidation and crosslink cell components into additional LAS carriers. With time and sufficient promotion by pH fluctuations or metal-complexing agents, DIP and LAS expand. DIP injures through heavy-metal inhibition of life processes and catalysis of autoxidation. Typically, carcinogenic initiators are protein denaturants, cell poisons, “foreign bodies” and autoxidation catalysts. These are DIP-initiating properties, and DIP may be a preneoplastic stage of carcinogenesis. A DIP-model interpretation is given for the growth of asbestos bodies. DIP is an inorganic parasite. It may envelope and attack phagocytized particles.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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