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.
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- CATEGORIES: Chemical used in hydraulic fracturing fluids | Household Toxin | Animal Toxin | Food Toxin | Natural Toxin | EAFUS (Everything Added to Food in the United States) | Inert Pesticide Ingredient USA - Food Use Permitted
- SUBSTANCE LINEAGE: Organic Compounds | Organooxygen Compounds | Carbohydrates and Carbohydrate Conjugates | Monosaccharides | Oxanes
- SYNONYMS: (+)-Glucose | Anhydrous dextrose | Cerelose | Cerelose 2001 | Clearsweet 95 | Clintose L | Corn sugar | CPC hydrate | D(+)-Glucose | Dextropur | Dextrose | Dextrosol | Glucodin | Glucolin | Glucose | Goldsugar | Grape sugar | Meritose | Roferose st | Staleydex 111 | Staleydex 95M | Tabfine 097(HS) | Vadex
- DESCRIPTION: Has been used in CSG, Hydraulic Fracturing Operations (Fracking) as - Unknown | Glucose is a monosaccharide containing six carbon atoms and an aldehyde group and is therefore referred to as an aldohexose. The glucose molecule can exist in an open-chain (acyclic) and ring (cyclic) form, the latter being the result of an intramolecular reaction between the aldehyde C atom and the C-5 hydroxyl group to form an intramolecular hemiacetal. In water solution both forms are in equilibrium and at pH 7 the cyclic one is the predominant. Glucose is a primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. In animals glucose arises from the breakdown of glycogen in a process known as glycogenolysis. Glucose is synthesized in the liver and kidneys from non-carbohydrate intermediates, such as pyruvate and glycerol, by a process known as gluconeogenesis.
- FORMULA: C6H12O6
- DATA SOURCES: DATA SOURCES: ARTICLE 4 | T3DB | PubChem | EPA in USA | US HOUSE OF REPRESENTATIVES | EAFUS | EPA USA - Pesticide Inerts
- LAST UPDATE: 28/04/2018
Mostly focused on Health Implications of Long Term Exposure to this substance
- POSSIBLE HEALTH CONSEQUENCES: High blood glucose (>7 mM) produces the symptoms of frequent urination, increased thirst, and increased hunger. Chronic exposure to high blood glucose (i.e. untreated diabetes) can cause many complications. Acute complications include diabetic ketoacidosis (characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath) and nonketotic hyperosmolar coma. Serious long-term complications include heart disease, stroke, kidney failure, foot ulcers and damage to the eyes. The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in diabetics are due to coronary artery disease. Other "macrovascular" diseases are stroke, and peripheral vascular disease. The primary microvascular complications of diabetes include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and potentially blindness. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplant. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from red blood cell destruction. |
- ACTION OF TOXIN: Very high serum levels of glucose are found in untreated diabetic (type I or type II) patients. Glucose in chronic excess causes toxic effects on the structure and function of many cells and organs, including the pancrease and pancreatic islet cells. Multiple biochemical pathways and mechanisms of action for glucose toxicity have been suggested. These include glyceraldehyde auto-oxidation, protein kinase C activation, methylglyoxal formation and glycation, hexosamine metabolism, sorbitol formation, and oxidative phosphorylation. All these pathways have in common the formation of reactive oxygen species that, in excess and over time, cause chronic oxidative stress, which in turn causes defective insulin gene expression and insulin secretion as well as increased apoptosis. Exposure of endothelial cells to high glucose causes GAPDH inhibition through reactive oxygen species-activated poly(ADP-ribosyl)ation of GAPDH by poly(ADP-ribose) polymerase. Three products from glucose metabolism: glyoxal, methylglyoxal, and 3-deoxyglucosone) form advanced glycation end products (AGEs) by reacting with amino groups on intracellular and extracellular proteins. AGEs play important roles in the pathogenesis of secondary complications of diabetes, especially with regard to microvascular disease in the retina, nerves, and kidney and likely islets. Glycated hemoglobin is a particularly important AGE. A 1% increase in absolute concentrations of glycated hemoglobin is associated with about 10-20% increase in cardiovascular disease risk. |
- TOXIN SITES OF ACTION IN CELL: "Endoplasmic reticulum", "Extracellular", "Golgi apparatus", "Lysosome", "Membrane"
- Additional Exposure Routes:
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