Disease relevance of Lathyrus neurotoxin

• Species differences in susceptibility are a unique feature associated with the neurotoxicity of beta-N-oxalyl-L-alpha,beta-diaminopropionic acid (L-ODAP), the Lathyrus sativus neurotoxin, and the excitotoxic mechanism proposed for its mechanism of toxicity does not account for this feature [1].
• beta-N-Oxalyl-L-alpha,beta-diaminopropionic acid (beta-L-ODAP) is an excitatory amino acid agonist found in the seeds of Lathyrus sativus that is believed to be the major causative agent in the pathology of human lathyrism [2].
• Prolonged oral administration of the Lathyrus sativus neurotoxin, L-3-oxalylamino-2-aminopropionic acid (OAP), to three young male squirrel monkeys at dose rates of 0.6 to 6.0 mg/g body weight/day produced no neurologic signs and no adverse effects other than depressed activity and occasional foaming at the mouth [3].
• Beta-N-oxalyl-L-alpha,beta-diaminopropionic acid (L-ODAP) toxicity has been associated with lathyrism; a spastic paraparesis caused by excessive dietary intake of the pulse Lathyrus sativus [4].
• Water stress and accumulation of beta-N-oxalyl-L-alpha,beta-diaminopropionic acid in grass pea (Lathyrus sativus) [5].

High impact information on Lathyrus neurotoxin

• Inhibition of tyrosine aminotransferase by beta-N-oxalyl-L-alpha,beta-diaminopropionic acid, the Lathyrus sativus neurotoxin [1].
• Induction of astrocyte glutamine synthetase activity by the Lathyrus toxin beta-N-oxalyl-L-alpha,beta-diaminopropionic acid (beta-L-ODAP) [6].
• Entry of beta-N-oxalyl-L-alpha,beta-diaminopropionic acid, the Lathyrus sativus neurotoxin into the central nervous system of the adult rat, chick and the rhesus monkey [7].
• Tissue distribution and metabolism of the Lathyrus sativus neurotoxin, L-3-oxalylamino-2-aminopropionic acid, in the squirrel monkey [8].
• The neurolathyrogen, beta-N-oxalyl-L-alpha,beta-diaminopropionic acid, is a potent agonist at 'glutamate preferring' receptors in the frog spinal cord [9].

Biological context of Lathyrus neurotoxin

• With the duration of PEG treatment, changes in the lipid peroxidation and activities of superoxide dismutase, catalase, peroxidase, and glutathione reductase as well as contents of hydrogen peroxide and beta-N-oxalyl-L-alpha,beta-diaminopropionic acid (ODAP) were assayed [5].
• Of the compounds tested, 3-N-oxalyl-L-2,3-diaminopropanoic acid (beta-ODAP), the causal agent of human neurolathyrism, exhibited an inhibitory activity on the NMDA receptor binding assay at a relatively high concentration (IC50: 4.7 x 10(-5)M) [10].

Anatomical context of Lathyrus neurotoxin

• Receptor interactions of beta-N-oxalyl-L-alpha,beta-diaminopropionic acid, the Lathyrus sativus putative excitotoxin, with synaptic membranes [11].
• Lathyrism is a non-progressive motor neuron disease produced by consumption of the excitatory amino acid, 3-N-oxalyl-L-2,3-diaminopropanoic acid (beta-ODAP) [12].
• It is characterized by severe muscular rigidity and paralysis of the lower limbs. beta-N-Oxalyl-L-alpha,beta-diaminopropionic acid is the principal toxin found in the seed [13].

Associations of Lathyrus neurotoxin with other chemical compounds

• Analysis of dencichine in Panax notoginseng by gas chromatography-mass spectrometry with ethyl chloroformate derivatization [14].

Analytical, diagnostic and therapeutic context of Lathyrus neurotoxin

• Hydrophilic interaction liquid chromatography with tandem mass spectrometry for the determination of underivatized dencichine (beta-N-oxalyl-L-alpha,beta-diaminopropionic acid) in Panax medicinal plant species [15].
• Liquid chromatographic determination of total and beta-N-oxalyl-L-alpha,beta-diaminopropionic acid in lathyrus sativus seeds using both refractive index and bioelectrochemical detection [16].

References