Substance Attributes
Carcinogenic Properties
Accumulating evidence points to cancer potential. Exercise caution with this substance, explore your exposure routes and consider complete avoidance. See further details under Toxins.
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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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Has known Side Effects
This is often the result of long or short term medication use. The same medication can have a range of side effects ranging from none at all to totally debilitating symptoms within different individuals. Reasons for this include individual genetics, individual detoxification capacity, nutrition status, duration of use and total number of medications being taken.
It becomes very difficult to establish clear causes of symptoms when multiple medications are being taken at once.
See SIDE EFFECTS LINKOUT at end of this profile.
These attributes are ONLY based on peer-reviewed evidence. See link to Data Sources below. Everyone benefits from knowing this stuff. Please Share.
- CATEGORIES: Food Additives with E Numbers | Flavour enhancers | Medication or Drug | Household Toxin | Food Toxin | Natural Toxin | Animal Toxin | Food Flavoring | EAFUS (Everything Added to Food in the United States) | Inert Pesticide Ingredient USA - Non Food Use Only | Medication Approved in USA
- SUBSTANCE LINEAGE: Organic Compounds | Organic Acids and Derivatives | Carboxylic Acids and Derivatives | Amino Acids, Peptides, and Analogues | Alpha Amino Acids
- SYNONYMS: 2-Aminoacetate | 2-Aminoacetic acid | Aciport | Amino-Acetate | Amino-Acetic acid | Aminoacetate | Aminoacetic acid | Aminoessigsaeure | Aminoethanoate | Aminoethanoic acid | G | Glicoamin | Gly | Glycin | Glycocoll | Glycolixir | Glycosthene | Glykokoll | Glyzin | Gyn-Hydralin | H2N-CH2-COOH | Hgly | Leimzucker | Padil
- DESCRIPTION: E Number: E640 | Food Additives with E Numbers used in Australia, NZ, UK and the EU. Over 400 in total. | Substance has been approved in: Australia and NZ | EU and UK | | Flavour enhancers | Glycine is a simple, nonessential amino acid, although experimental animals show reduced growth on low-glycine diets. The average adult ingests 3 to 5 grams of glycine daily. Glycine is involved in the body's production of DNA, phospholipids and collagen, and in release of energy. Glycine levels are effectively measured in plasma in both normal patients and those with inborn errors of glycine metabolism. Nonketotic hyperglycinaemia (OMIM 606899) is an autosomal recessive condition caused by deficient enzyme activity of the glycine cleavage enzyme system (EC 2.1.1.10). The glycine cleavage enzyme system comprises four proteins: P-, T-, H- and L-proteins (EC 1.4.4.2, EC 2.1.2.10 and EC 1.8.1.4 for P-, T- and L-proteins). Mutations have been described in the GLDC (OMIM 238300), AMT (OMIM 238310), and GCSH (OMIM 238330) genes encoding the P-, T-, and H-proteins respectively. The glycine cleavage system catalyses the oxidative conversion of glycine into carbon dioxide and ammonia, with the remaining one-carbon unit transferred to folate as methylenetetrahydrofolate. It is the main catabolic pathway for glycine and it also contributes to one-carbon metabolism. Patients with a deficiency of this enzyme system have increased glycine in plasma, urine and cerebrospinal fluid (CSF) with an increased CSF: plasma glycine ratio. (A3412). t is also a fast inhibitory neurotransmitter.
- COMMENTS:

- FORMULA: C2H5NO2
- DATA SOURCES: DATA SOURCES: ARTICLE 4 | CPDB | T3DB | PubChem | Flavornet | FSANZ and FSA | EAFUS | EPA USA - Pesticide Inerts | Drugbank | USA FDA APPROVED DRUG PRODUCTS
- LAST UPDATE: 28/04/2018
Health Associations
Mostly focused on Health Implications of Long Term Exposure to this substance
- SYMPTOMS:
- POSSIBLE HEALTH CONSEQUENCES: Chronically high levels of glycine are associated with at least 12 inborn errors of metabolism including: Citrullinemia Type I, Hyperglycinemia, non-ketotic, Hyperprolinemia Type I, Hyperprolinemia Type II, Iminoglycinuria, Isovaleric Aciduria, Malonic Aciduria, Methylmalonic Aciduria, Methylmalonic Aciduria Due to Cobalamin-Related Disorders, Non Ketotic Hyperglycinemeia, Prolinemia Type II, Propionic academia and Short Chain Acyl CoA Dehydrogenase Deficiency (SCAD Deficiency). | Hepatic
- ACTION OF TOXIN: In the CNS, there exist strychnine-sensitive glycine binding sites as well as strychnine-insensitive glycine binding sites. The strychnine-insensitive glycine-binding site is located on the NMDA receptor complex. The strychnine-sensitive glycine receptor complex is comprised of a chloride channel and is a member of the ligand-gated ion channel superfamily. The putative antispastic activity of supplemental glycine could be mediated by glycine's binding to strychnine-sensitive binding sites in the spinal cord. This would result in increased chloride conductance and consequent enhancement of inhibitory neurotransmission. The ability of glycine to potentiate NMDA receptor-mediated neurotransmission raised the possibility of its use in the management of neuroleptic-resistant negative symptoms in schizophrenia.
Animal studies indicate that supplemental glycine protects against endotoxin-induced lethality, hypoxia-reperfusion injury after liver transplantation, and D-galactosamine-mediated liver injury. Neutrophils are thought to participate in these pathologic processes via invasion of tissue and releasing such reactive oxygen species as superoxide. In vitro studies have shown that neutrophils contain a glycine-gated chloride channel that can attenuate increases in intracellular calcium and diminsh neutrophil oxidant production. This research is ealy-stage, but suggests that supplementary glycine may turn out to be useful in processes where neutrophil infiltration contributes to toxicity, such as ARDS. | - TOXIN SITES OF ACTION IN CELL: "Extracellular", "Lysosome", "Membrane", "Mitochondria", "Peroxisome"
- Additional Exposure Routes: Supplemental glycine may have antispastic activity. Very early findings suggest it may also have antipsychotic activity as well as antioxidant and anti-inflammatory activities.
SEE MEDICATION SIDE EFFECTS
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