Metabolic Interference or Disruption
Interferes with human metabolism. This can be a very serious thing. Some of these interference mechanics are well established. However, often long term effects and health consequences remain largely unknown. Additionally an emerging area of concern and one that is not currently studied, is the combined synergistic effects these metabolically disrupting chemicals have on human health.
Metabolic interference happens when the substance produces highly reactive and often damaging intermediates during detoxification or when the substance binds to specific enzymes, important structural groups on molecules, receptors and membranes or targets DNA or mimics key nutrients.
These attributes are ONLY based on peer-reviewed evidence. See link to Data Sources below. Everyone benefits from knowing this stuff. Please Share.
- CATEGORIES: Pesticide | Synthetic Toxin | PESTICIDE active ingredient | organic | fungicide | Pesticide or Plant Growth Regulator Approved in Australia | Pesticide approved in USA (California) | Pesticide approved or pending approval in EU
- SUBSTANCE LINEAGE: Organic Compounds | Heterocyclic Compounds | Benzodioxoles | | Benzodioxoles
- SYNONYMS: 3-(2,2-Difluoro-benzodioxol-4-yl)-4-cyanopyrrole | Fludioxonil | 4-(2,2-difluoro-1,3-benzodioxol-4-yl)-1H-pyrrole-3-carbonitrile
- DESCRIPTION: Fludioxonil is a fungicide seed treatment for control of a range of diseases including Fusarium, Rhizoctonia and Alternaria. It has a non-systemic action with long residual activity. It also inhibits transport-associated phosphorylation of glucose, reducing mycelial growth.
- COMMENTS: Residues of this pesticide are tested for on Australian Foods | Pesticide approved in Australia
- FORMULA: C12H6F2N2O2
- DATA SOURCES: DATA SOURCES: T3DB | PubChem | Consolidated Pesticide Information Dataset (CPI) from the USA EPA | Compendium of Pesticide Common Names | APVMA | DPR | EU Pesticides
- LAST UPDATE: 28/04/2018
Mostly focused on Health Implications of Long Term Exposure to this substance
- POSSIBLE HEALTH CONSEQUENCES: | Organic nitriles are converted into cyanide ions through the action of cytochrome P450 enzymes in the liver. Cyanide is rapidly absorbed and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (L96)
- ACTION OF TOXIN: Organic nitriles decompose into cyanide ions both in vivo and in vitro. Consequently the primary mechanism of toxicity for organic nitriles is their production of toxic cyanide ions or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (L97) |
- TOXIN SITES OF ACTION IN CELL: "Cytosol", "Membrane", "Plasma Membrane"
- Additional Exposure Routes: This is a man-made compound that is used as a pesticide.
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