Oxalyldiaminopropionic acid

Oxalyldiaminopropionic acid

Names
IUPAC name 3-[(Carboxycarbonyl)amino]alanine
Other names Dencichin β-Oxalylaminoalanine β-N-Oxalyl-α,β-diaminopropionic acid β-N-oxalylamino-L-alanine (L-BOAA)
Identifiers
CAS Number	7554-90-7 N 5302-45-4 (S) N
3D model (Jmol)	Interactive image
3DMet	B00693
Abbreviations	BOAA ODAP β-ODAP
ChEBI	CHEBI:16399 N
ChemSpider	389238 (S) N 2270 (rac) N
KEGG	C04209 N
MeSH	oxalyldiaminopropionic+acid
PubChem CID	2360 440259 (S)
InChI InChI=1S/C5H8N2O5/c6-2(4(9)10)1-7-3(8)5(11)12/h2H,1,6H2,(H,7,8)(H,9,10)(H,11,12)/t2-/m0/s1 N Key: NEEQFPMRODQIKX-REOHCLBHSA-N N
SMILES C([C@@H](C(=O)O)N)NC(=O)C(=O)O
Properties
Chemical formula	C5H8N2O5
Molar mass	176.13 g·mol−1
Related compounds
Related compounds	Beta-Methylamino-L-alanine
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
N  (what is YN ?)
Infobox references

Oxalyldiaminopropionic acid (ODAP) is a structural analogue of the neurotransmitter glutamate found in the grass pea Lathyrus sativus. It is the neurotoxin responsible for the motor neuron degeneration syndrome lathyrism.

ODAP is found in the seeds of the legume L. sativus, a grass pea plant, at a constant concentration of .5%.L. sativus can be found in areas of Southern, Central, and Eastern Europe, the Mediterranean Basin, Iraq and Afghanistan as well as areas of Asia and Africa.

In some regions, including the Indian subcontinent, Bangladesh, Ethiopia and Nepal, the grass pea has become a staple food item. The plant has a high tolerance of environmental conditions which results in it being the only available food source in times of famine or drought. Following these several month droughts, neurolathyrism epidemics may occur. The last instance of such an epidemic (as of 2013) was in Ethiopia during the 1995-1997 drought during which 2000 people were crippled.

ODAP is an agonist of the ionotropicAMPA glutamate receptor. It is known to cause neurolathyrism in humans, a motor neuron degenerative disease characterized by degeneration of pyramidal-tract neurons in the spinal cord and in the area of the cortex controlling the legs, resulting in lower-body paralysis. There is not one direct explanation as to how ODAP causes neurolathyrism; however, there has been evidence to support a few biological effects. One reason why the mechanism of action is not entirely clear may be because, so far, a good animal model for the effect of ODAP in humans has not been found. The LD₅₀ is also unknown.

ODAP activates AMPA receptors which can induce excitotoxicity, or an overstimulation of glutamate receptors. The release of too much glutamate, either at once or over a prolonged period of time, will lead to increased levels of Ca2+
in the cytoplasm. Since Ca2+
is the signaling molecule for the release of glutamate into the synapse, this can result in potentiation of the glutamate release cycle and the spread of excitotoxic damage to neighboring neurons. Inside the neuron, the extra Ca2+
will leave the cytoplasm and enter either the or the endoplasmic reticulum (ER), which can lead to accumulation of misfolded or unfolded proteins in the ER and ultimately cell death in both cases. In addition to acting as an agonist there is evidence to show that ODAP is transported into the cell by an antiporter that simultaneously transports glutamate into the synapse.