Ravindranath, V (2002) Neurolathyrism: mitochondrial dysfunction in excitotoxicity mediated by l-β-oxalyl aminoalanine. Neurochemistry International, 40 (6). pp. 505-509.

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Abstract

β-N-Oxalyl amino-l-alanine (l-BOAA); synonym β-N-oxalyl-α,β-diaminopropionic acid (β-ODAP) is a naturally occurring non-protein amino acid present in the chickling pea from the plant Lathyrus sativus grown in drought prone areas. Ingestion of l-BOAA as a staple diet results in a progressive neurodegenerative condition, neurolathyrism, a form of motor neuron disease which affects the upper motor neurons and anterior horn cells of the lumbar spinal cord. l-BOAA is an excitatory acid and acts as an agonist at the AMPA receptor. One of the primary effects of l-BOAA toxicity is the inhibition of mitochondrial complex I selectively in the motor cortex and lumbar spinal cord. Recent evidence has suggested that the mitochondrial dysfunction is a consequence of oxidation protein thiol groups as a result of generation of reactive oxygen species. Mitochondrial complex I is highly to vulnerable to inactivation through oxidation of vital sulfhydryl groups. Thiol antioxidants such as α-liopic acid offer a method of protecting mitochondrial function. A common mechanism involving oxidation of protein thiol groups may underlie neurodegeneration occurring through mitochondrial dysfunction induced by excitatory amino acid.

Item Type:	Article
Subjects:	Neurodegenerative Disorders Neuro-Oncological Disorders Neurocognitive Processes Neuronal Development and Regeneration Informatics and Imaging Genetics and Molecular Biology
Depositing User:	Dr. D.D. Lal
Date Deposited:	05 Feb 2020 09:19
Last Modified:	05 Feb 2020 09:19
URI:	http://nbrc.sciencecentral.in/id/eprint/542

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