Disease relevance of beta-N-oxalylamino-L-alanine

• It has been suggested that beta-N-oxalylamino-L-alanine, a non-protein amino acid present in the Lathyrus Sativus seeds, may play a role in the etiopathogenesis of neurolathyrism, a toxic form of motor neuron disease clinically characterized by a severe spastic paraparesis [1].
• Interestingly, a mathematical analysis applied to the time course and dose curve of beta-N-oxalylamino-L-alanine toxicity suggested that even for very low concentrations of the amino acid it is theoretically possible to predict a time-dependent effect [1].
• Recent studies have implicated the ingestion of the structurally related plant excitotoxins, beta-N-methylamino-L-alanine (BMAA), and beta-N-oxalylamino-L-alanine (BOAA), in the pathogenesis of two human motor system diseases, the amyotrophic lateral sclerosis-Parkinsonism-dementia complex of Guam (Guam ALS-PD), and lathyrism, respectively [2].

High impact information on beta-N-oxalylamino-L-alanine

• Therefore, in cerebellar granule cells, beta-N-methylamino-L-alanine and beta-N-oxalylamino-L-alanine induce death over 12-72 h of exposure via a mechanism that involves both necrotic- and apoptotic-like cell death [3].
• In the present study the subacute effects of beta-N-oxalylamino-L-alanine (BOAA) and beta-N-methylamino-L-alanine (BMAA) on CNS monoamine neurons in rats were investigated following intracisternal injections or local intracerebral administration into substantia nigra [4].
• beta-N-Oxalylamino-L-alanine: action on high-affinity transport of neurotransmitters in rat brain and spinal cord synaptosomes [5].
• Differential effect of beta-N-oxalylamino-L-alanine, the Lathyrus sativus neurotoxin, and (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate on the excitatory amino acid and taurine levels in the brain of freely moving rats [6].
• Apoptosis induced by beta-N-oxalylamino-L-alanine on a motoneuron hybrid cell line [1].

Chemical compound and disease context of beta-N-oxalylamino-L-alanine

• Lathyrism is a disorder of the central motor system, induced by heavy consumption of the grass-pea, Lathyrus sativus an environmentally tolerant legume containing the neurotoxic excitatory amino acid beta-N-oxalylamino-L-alanine (BOAA) [7].
• Thus, domoic acid, a KAIN receptor agonist, has probably been the cause of severe neurologic illness in people who consumed domoic acid poisoned food. beta-N-oxalylaminoalanine (beta-ODAP), an AMPA receptor agonist, has been associated with lathyrism, a spastic paraparesis caused by dietary intake of Lathyrus sativus [8].

Anatomical context of beta-N-oxalylamino-L-alanine

• Neuronal damage induced by beta-N-oxalylamino-L-alanine, in the rat hippocampus, can be prevented by a non-NMDA antagonist, 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline [9].
• The L-isomer of beta-N-methylamino-L-alanine (BMAA), present in free form in seed of Cycas circinalis, elicits in spinal cord cultures a pattern of acute postsynaptic neuronal vacuolation comparable to that induced by beta-N-oxalylamino-L-alanine (BOAA), an excitotoxic amino acid of greater potency isolated from seed of Lathyrus sativus [10].

Associations of beta-N-oxalylamino-L-alanine with other chemical compounds

• Neurolathyrism is a degenerative disorder due to an excessive consumption of Lathyrus sativus (LS) seeds, which contain the neurotoxic amino acid beta-N-oxalylamino-L-alanine [11].

Gene context of beta-N-oxalylamino-L-alanine

• The effect of beta-N-oxalylamino-L-alanine on glutamine synthetase activity and the transport of D-3 H-aspartate in rat brain in vitro [12].

Analytical, diagnostic and therapeutic context of beta-N-oxalylamino-L-alanine

• Early alterations in mRNAs encoding neurotrophins and stress proteins were investigated following intracerebroventricular injections of beta-N-oxalylamino-L-alanine (BOAA) and beta-N-methylamino-L-alanine (BMAA) in adult rats using in situ hybridization [13].

References