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Tyramine

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Tyramine
Names
IUPAC name
4-(2-aminoethyl)phenol
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
ECHA InfoCard 100.000.106 Edit this at Wikidata
KEGG
MeSH Tyramine
UNII
  • InChI=1S/C8H11NO/c9-6-5-7-1-3-8(10)4-2-7/h1-4,10H,5-6,9H2 checkY
    Key: DZGWFCGJZKJUFP-UHFFFAOYSA-N checkY
  • InChI=1/C8H11NO/c9-6-5-7-1-3-8(10)4-2-7/h1-4,10H,5-6,9H2
    Key: DZGWFCGJZKJUFP-UHFFFAOYAB
  • Oc1ccc(cc1)CCN
Properties
C8H11NO
Molar mass 137.179 g/mol[1]
Appearance colorless solid
Density 1.20 g/cm 3[2]
Melting point 164 to 165 °C (327 to 329 °F; 437 to 438 K)[3]
Boiling point 205 to 207 °C (401 to 405 °F; 478 to 480 K) at 25 mmHg; 166 °C at 2 mmHg[3]
1 g in 95 mL at 15 °C[3]
Acidity (pKa) 9.74 (OH); 10.52 (NH3+) [4]
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)

Tyramine (4-hydroxyphenethylamine; para-tyramine, mydrial or uteramin) is a naturally occurring monoamine compound and trace amine derived from the amino acid tyrosine.[1] Tyramine acts as a catecholamine releasing agent. Notably, it is unable to cross the blood-brain barrier, resulting in only non-psychoactive peripheral sympathomimetic effects. A hypertensive crisis can result, however, from ingestion of tyramine-rich foods in conjunction with monoamine oxidase inhibitors (MAOIs).

Occurrence

Tyramine occurs widely in plants[5] and animals, and is metabolized by the enzyme monoamine oxidase. In foods, it often is produced by the decarboxylation of tyrosine during fermentation or decay. Foods containing considerable amounts of tyramine include meats that are potentially spoiled or pickled, aged, smoked, fermented, or marinated (some fish, poultry, and beef); most pork (except cured ham). Other foods containing considerable amounts of tyramine are chocolate; alcoholic beverages; and fermented foods, such as most cheeses (except ricotta, cottage, cream and Neufchâtel cheeses), sour cream, yogurt, shrimp paste, soy sauce, soybean condiments, teriyaki sauce, tempeh, miso soup, sauerkraut, kimchi, broad (fava) beans, green bean pods, Italian flat (Romano) beans, snow peas, edamame, avocados, bananas, pineapple, eggplants, figs, red plums, raspberries, peanuts, Brazil nuts, coconuts, processed meat, yeast, an array of cacti and the holiday plant mistletoe.

Physical effects and pharmacology

Evidence for the presence of tyramine in the human brain has been confirmed by postmortem analysis.[6] Additionally, the possibility that tyramine acts directly as a neurotransmitter was revealed by the discovery of a G protein-coupled receptor with high affinity for tyramine, called TAAR1.[7][8] The TAAR1 receptor is found in the brain, as well as peripheral tissues, including the kidneys.[9]

Tyramine is physiologically metabolized by MAOA. In humans, if monoamine metabolism is compromised by the use of monoamine oxidase inhibitors (MAOIs) and foods high in tyramine are ingested, a hypertensive crisis can result, as tyramine also can displace stored monoamines, such as dopamine, norepinephrine, and epinephrine, from pre-synaptic vesicles.

The first signs of this were discovered by a neurologist who noticed his wife, who at the time was on MAOI medication, had severe headaches when eating cheese.[10] For this reason, the crisis is still called the "cheese effect" or "cheese crisis", though other foods can cause the same problem.[11]: 30–31 

Most processed cheeses do not contain enough tyramine to cause hypertensive effects, although some aged cheeses (such as Stilton) do.[12][13]

A large dietary intake of tyramine (or a dietary intake of tyramine while taking MAO inhibitors) can cause the tyramine pressor response, which is defined as an increase in systolic blood pressure of 30 mmHg or more. The displacement of norepinephrine (noradrenaline) from neuronal storage vesicles by acute tyramine ingestion is thought to cause the vasoconstriction and increased heart rate and blood pressure of the pressor response. In severe cases, adrenergic crisis can occur.[medical citation needed] Although the mechanism is unclear, tyramine ingestion also triggers migraines in sensitive individuals. Vasodilation, dopamine, and circulatory factors are all implicated in migraine. Double-blind trials suggest that the effects of tyramine on migraines may be adrenergic.[14] Migraineurs are over-represented among those with inadequate natural monoamine oxidase, resulting in similar problems individuals taking MAO inhibitors. Many migraine triggers are high in tyramine.[15]

If one has had repeated exposure to tyramine, however, there is a decreased pressor response; tyramine is degraded to octopamine, which is subsequently packaged in synaptic vesicles with norepinephrine (noradrenaline).[citation needed] Therefore, after repeated tyramine exposure, these vesicles contain an increased amount of octopamine and a relatively reduced amount of norepinephrine. When these vesicles are secreted upon tyramine ingestion, there is a decreased pressor response, as less norepinephrine is secreted into the synapse, and octopamine does not activate alpha or beta adrenergic receptors.[medical citation needed]

When using a MAO inhibitor (MAOI), the intake of approximately 10 to 25 mg of tyramine is required for a severe reaction compared to 6 to 10 mg for a mild reaction.[medical citation needed]

Research reveals a possible link between migraine and elevated levels of tyramine. A 2007 review published in Neurological Sciences[16] presented data showing migraine and cluster headaches are characterised by an increase of circulating neurotransmitters and neuromodulators (including tyramine, octopamine and synephrine) in the hypothalamus, amygdala and dopaminergic system.

Biosynthesis

Biochemically, tyramine is produced by the decarboxylation of tyrosine via the action of the enzyme tyrosine decarboxylase.[17] Tyramine can, in turn, be converted to methylated alkaloid derivatives N-methyltyramine, N,N-dimethyltyramine (hordenine), and N,N,N-trimethyltyramine (candicine).

  • Tyramine
    Tyramine
  • N-Methyltyramine
    N-Methyltyramine
  • N,N-Dimethyltyramine (hordenine)
    N,N-Dimethyltyramine (hordenine)
  • N,N,N-Trimethyltyramine (candicine)
    N,N,N-Trimethyltyramine (candicine)

In humans, tyramine is produced from tyrosine, as shown in the following diagram.

Biosynthetic pathways for catecholamines and trace amines in the human brain[18][19][20]
The image above contains clickable links
In humans, catecholamines and phenethylaminergic trace amines are derived from the amino acid L-phenylalanine.

Chemistry

In the laboratory, tyramine can be synthesized in various ways, in particular by the decarboxylation of tyrosine.[21][22][23]

United States

Tyramine is not scheduled at the federal level in the United States and is therefore legal to buy, sell, or possess.[24]

Status in Florida

Tyramine is a Schedule I controlled substance, categorized as a hallucinogen, making it illegal to buy, sell, or possess in the state of Florida without a license at any purity level or any form whatever. The language in the Florida statute says tyramine is illegal in "any material, compound, mixture, or preparation that contains any quantity of [tyramine] or that contains any of [its] salts, isomers, including optical, positional, or geometric isomers, and salts of isomers, if the existence of such salts, isomers, and salts of isomers is possible within the specific chemical designation".[25] This ban is likely the product of lawmakers overly eager to ban substituted phenethylamines, which tyramine is, in the mistaken belief that ring-substituted phenethylamines are hallucinogenic drugs like the 2C series of psychedelic substituted phenethylamines. The further banning of tyramine's optical isomers, positional isomers, or geometric isomers, and salts of isomers where they exist, means that meta-tyramine and phenylethanolamine, a substance found in every living human body, and other common, non-hallucinogenic substances are also illegal in to buy, sell or possess in Florida.[citation needed]

See also

References

  1. ^ a b PubChem
  2. ^ Andersen A. M. (1977). "The crystal and molecular structure of tyramine hydrochloride". Acta Chem. Scandinavica B. 31: 162–166.
  3. ^ a b c The Merck Index, 10th Ed. (1983), p.1405, Rahway: Merck & Co.
  4. ^ Kappe, T. (1965). "Ultraviolet Absorption Spectra and Apparent Acidic Dissociation Constants of Some Phenolic Amines 1". Journal of Medicinal Chemistry. 8: 368–374. doi:10.1021/jm00327a018Template:Inconsistent citations{{cite journal}}: CS1 maint: postscript (link)
  5. ^ T. A. Smith (1977) Phytochem. 16 9-18.
  6. ^ Philips, Rozdilsky, Boulton (February 1978). "Evidence for the presence of m-tyramine, p-tyramine, tryptamine, and phenylethylamine in the rat brain and several areas of the human brain". Biological Psychiatry. 13 (1): 51–57. PMID 623853.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  7. ^ Navarro, Gilmour, Lewin (10 July 2006). "A Rapid Functional Assay for the Human Trace Amine-Associated Receptor 1 Based on the Mobilization of Internal Calcium". J Biomol Screen. 11 (6): 668–693. doi:10.1177/1087057106289891. PMID 16831861.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ Liberles, Buck (10 August 2006). "A second class of chemosensory receptors in the olfactory epithelium". Nature. 441 (7103): 645–650. doi:10.1038/nature05066. PMID 16878137.
  9. ^ Xie, Westmoreland, Miller (May 2008). "Modulation of monoamine transporters by common biogenic amines via trace amine-associated receptor 1 and monoamine autoreceptors in human embryonic kidney 293 cells and brain synaptosomes". J. Pharm. 441 (2): 629–640. doi:10.1124/jpet.107.135079. PMID 18310473.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ Sathyanarayana Rao TS and Vikram K. Yeragani VK (2009) Hypertensive crisis and cheese Indian J Psychiatry. 51(1): 65–66.
  11. ^ E. Siobhan Mitchell Antidepressants, chapter in Drugs, the Straight Facts, edited by David J. Triggle. 2004, Chelsea House Publishers
  12. ^ Stahl SM, Felker A (2008). "Monoamine oxidase inhibitors: a modern guide to an unrequited class of antidepressants". Cns Spectrums. 13 (10): 855–870. PMID 18955941.
  13. ^ Tyramine-restricted Diet 1998, W.B. Saunders Company.
  14. ^ http://www.bmj.com/content/1/6070/1191?variant=abstract
  15. ^ http://www.headaches.org/headache-sufferers-diet/
  16. ^ D'Andrea, G; Nordera, GP; Perini, F; Allais, G; Granella, F (May 2007). "Biochemistry of neuromodulation in primary headaches: focus on anomalies of tyrosine metabolism". Neurological Sciences. 28, Supplement 2 (S2): S94–S96. doi:10.1007/s10072-007-0758-4. PMID 17508188Template:Inconsistent citations{{cite journal}}: CS1 maint: postscript (link)
  17. ^ Tyrosine metabolism - Reference pathway, Kyoto Encyclopedia of Genes and Genomes (KEGG)
  18. ^ Broadley KJ (March 2010). "The vascular effects of trace amines and amphetamines". Pharmacology & Therapeutics. 125 (3): 363–375. doi:10.1016/j.pharmthera.2009.11.005. PMID 19948186.
  19. ^ Lindemann L, Hoener MC (May 2005). "A renaissance in trace amines inspired by a novel GPCR family". Trends in Pharmacological Sciences. 26 (5): 274–281. doi:10.1016/j.tips.2005.03.007. PMID 15860375.
  20. ^ Wang X, Li J, Dong G, Yue J (February 2014). "The endogenous substrates of brain CYP2D". European Journal of Pharmacology. 724: 211–218. doi:10.1016/j.ejphar.2013.12.025. PMID 24374199.
  21. ^ G. Barger (1909). "CXXVII.?Isolation and synthesis of p-hydroxyphenylethylamine, an active principle of ergot soluble in water". J. Chem. Soc. 95: 1123. doi:10.1039/ct9099501123.
  22. ^ Waser, Ernst (1925). "Untersuchungen in der Phenylalanin-Reihe VI. Decarboxylierung des Tyrosins und des Leucins". Helvetica Chimica Acta. 8: 758–773. doi:10.1002/hlca.192500801106.
  23. ^ Buck, Johannes S. (1933). "Reduction of Hydroxymandelonitriles. A New Synthesis of Tyramine". Journal of the American Chemical Society. 55 (8): 3388–3390. doi:10.1021/ja01335a058.
  24. ^ §1308.11 Schedule I
  25. ^ Florida Statutes - Chapter 893 - DRUG ABUSE PREVENTION AND CONTROL
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