Article

A REVIEW ON ANALOGUES OF BETA ODAP IN TREATMENT OF NEUROLATHYRISM SHOWING DOCKING AFFINITY
Gellela Harikiran* , Chiranjeevi Shankar, V. Vasanth Kumar, CH. Swarnalatha, K. Sowjanya, A. Navya

Details

Author

Gellela Harikiran*

ISSN

Applied

DOI

https://doi.org/10.5281/zenodo.3266262

Published on

Jun 13, 2019

Abstract

Lathyrism or neurolathyrism is a neurological disease of humans and domestic animals, caused by eating certain legumes like Lathyrus sativus also known as Grass pea, containing the toxin β-oxalyl-L-α,β-diaminopropionic acid (ODAP). This consumption containing high concentrations of the glutamate analogue neurotoxin beta ODAP causes paralysis by binding at AMPA selective ionotropic glutamate receptors and blocking glutamate transport in the neural milieu and triggering excitotoxic degeneration of neurons, and may involve pyramidal tracts producing signs of upper motor neuron damage. The toxin may also cause aortic aneurysm. ODAP is a poison of mitochondria, leading to excess cell death, especially in motor neurons Children can additionally develop bone deformity and reduced brain development. Recent research suggests that sulfur amino acids have a protective effect against the toxicity of ODAP by applying docking property some researchers have proved to minimise the effect of toxic by developing analogues of beta ODAP with competitively binding to the respective receptor and decrease the neurotoxicity Carboxymethyl alpha, betadiaminopropanoic acid (CMDAP) N-acetyl-alpha, beta- diaminopropanoic acid (ADAP), Carboxymethylcysteine (CMC). Ligand binding studies demonstrated that all the three compounds were effective to in displacing glutamate. The maximum inhibition was 92% for CMDAP, 61% for ADAP, 65% for CMC. These data indicate that analogues of beta-ODAP may interact with glutamate receptors without producing neurotoxicity

Keywords

Neurolathyrism, Docking, Motor degeneration, Beta ODAP.

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