The neurotoxicity of beta-N-oxalyl-L-alphabeta-diaminopropionic acid, the neurotoxin from the pulse Lathyrus sativus.

Abstract

Intraperitoneal administration of beta-N-oxalyl-l-alphabeta-diaminopropionic acid, the neurotoxin from Lathyrus sativus, to 12-day-old rats causes typical convulsions within 10min. There is a striking accumulation of glutamine in the brain, and chronic ammonia toxicity is indicated. There are no changes in the amounts of urea, aspartic acid and glutamic acid in the brain. Adult rats, even when injected with a dose of excess of beta-N-oxalyl-l-alphabeta-diaminopropionic acid, do not develop symptoms, and there are no changes in the amounts of glutamine or ammonia in the brain. A significant concentration of beta-N-oxalyl-l-alphabeta-diaminopropionic acid can be detected in the brain of the young rat but not in that of the adult animal. It is concluded that beta-N-oxalyl-l-alphabeta-diaminopropionic acid interferes with the ammonia-generating or -fixing mechanisms in the brain and leads to chronic ammonia toxicity.