<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">1694</id>
  <title>T3D1690</title>
  <common-name>Beta-Aminopropionitrile</common-name>
  <description>beta-Aminopropionitrile is a toxic amino-acid derivative. On an unusual case of the Cantrell-sequence in a premature infant with associated dysmelia, aplasia of the right kidney, cerebellar hypoplasia and circumscribed aplasia of the cutis, maternal history suggested an occupational exposure to aminopropionitriles prior to pregnancy. The characteristic features of the Cantrell-sequence--anterior thoraco-abdominal wall defect with ectopia cordis and diaphragm, sternum, pericardium, and heart defects--have been observed in animals following maternal administration of beta-aminopropionitrile. Some species of lathyrus (chickling pea, Lathyrus sativus- related), notably Lathyrus odoratus, are unable to induce human lathyrism but contain beta-aminopropionitrile, that induces pathological changes in bone (osteolathyrism) and blood vessels (angiolathyrism) of experimental animals without damaging the nervous system. The administration of beta-aminopropionitrile has been proposed for pharmacological control of unwanted scar tissue in human beings. beta-Aminopropionitrile is a reagent used as an intermediate in the manufacture of beta-alanine and pantothenic acid. (A11439, A11440, A11441)</description>
  <cas>151-18-8</cas>
  <pubchem-id>1647</pubchem-id>
  <chemical-formula>C3H6N2</chemical-formula>
  <weight>70.053100</weight>
  <appearance>White powder.</appearance>
  <melting-point>&lt; 25°C</melting-point>
  <boiling-point nil="true"/>
  <density nil="true"/>
  <solubility></solubility>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Oral (L96) ; inhalation (L96) ; dermal (L96)</route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>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)</mechanism-of-toxicity>
  <metabolism>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)</metabolism>
  <toxicity nil="true"/>
  <lethaldose>206 to 300 milligrams for an adult human (cyanide salts). (T86)</lethaldose>
  <carcinogenicity>No indication of carcinogenicity to humans (not listed by IARC).</carcinogenicity>
  <use-source>beta-Aminopropionitrile is a reagent used as an intermediate in the manufacture of beta-alanine and pantothenic acid.</use-source>
  <min-risk-level nil="true"/>
  <health-effects>Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma, seizures, apnea, cardiac arrest and death. Chronic inhalation of cyanide causes breathing difficulties, chest pain, vomiting, blood changes, headaches, and enlargement of the thyroid gland. Skin contact with cyanide salts can irritate and produce sores. (L96, L97)</health-effects>
  <symptoms>Cyanide poisoning is identified by rapid, deep breathing and shortness of breath, general weakness, giddiness, headaches, vertigo, confusion, convulsions/seizures and eventually loss of consciousness. (L96, L97)</symptoms>
  <treatment>Antidotes to cyanide poisoning include hydroxocobalamin and sodium nitrite, which release the cyanide from the cytochrome system, and rhodanase, which is an enzyme occurring naturally in mammals that combines serum cyanide with thiosulfate, producing comparatively harmless thiocyanate. Oxygen therapy can also be administered. (L97)</treatment>
  <created-at type="dateTime">2009-06-22T16:08:27Z</created-at>
  <updated-at type="dateTime">2014-12-24T20:24:27Z</updated-at>
  <interacting-proteins>Thiosulfate sulfurtransferase (Q16762) 3-mercaptopyruvate sulfurtransferase (P25325) (L96)</interacting-proteins>
  <wikipedia nil="true"/>
  <uniprot-id nil="true"/>
  <kegg-compound-id>C05670</kegg-compound-id>
  <omim-id></omim-id>
  <chebi-id>27413</chebi-id>
  <biocyc-id>BETA-AMINOPROPIONITRILE</biocyc-id>
  <ctd-id>D000629</ctd-id>
  <stitch-id>Aminopropionitrile</stitch-id>
  <drugbank-id nil="true"/>
  <pdb-id nil="true"/>
  <actor-id nil="true"/>
  <organism nil="true"/>
  <export type="boolean">true</export>
  <metabolizing-proteins>Thiosulfate sulfurtransferase (Q16762) 
3-mercaptopyruvate sulfurtransferase (P25325) 
(L96)</metabolizing-proteins>
  <transporting-proteins nil="true"/>
  <moldb-smiles>NCCC#N</moldb-smiles>
  <moldb-formula>C3H6N2</moldb-formula>
  <moldb-inchi>InChI=1S/C3H6N2/c4-2-1-3-5/h1-2,4H2</moldb-inchi>
  <moldb-inchikey>InChIKey=AGSPXMVUFBBBMO-UHFFFAOYSA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">70.0931</moldb-average-mass>
  <moldb-mono-mass type="decimal">70.053098202</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp nil="true"/>
  <hmdb-id>HMDB04101</hmdb-id>
  <chembl-id>CHEMBL1618272</chembl-id>
  <chemspider-id>21241485</chemspider-id>
  <structure-image-file-name nil="true"/>
  <structure-image-content-type nil="true"/>
  <structure-image-file-size type="integer" nil="true"/>
  <structure-image-updated-at type="dateTime" nil="true"/>
  <biodb-id nil="true"/>
  <synthesis-reference>Smolin, Edwin M.; Beegle, L. Clair. Continuous high-pressure synthesis of 3-aminopropionitrile. Journal of Industrial and Engineering Chemistry (Washington, D. C.) (1958), 50 1115-18.</synthesis-reference>
  <structure-image-caption nil="true"/>
</compound>
