Cheema P S, Malathi K, Padmanaban G, Sarma P S
Biochem J. 1969 Mar;112(1):29-33. doi: 10.1042/bj1120029.
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.
向12日龄大鼠腹腔注射来自山黧豆的神经毒素β-N-草酰-L-α,β-二氨基丙酸，10分钟内会引发典型惊厥。大脑中谷氨酰胺显著蓄积，提示存在慢性氨中毒。大脑中尿素、天冬氨酸和谷氨酸的含量无变化。成年大鼠即使注射过量的β-N-草酰-L-α,β-二氨基丙酸也不会出现症状，大脑中谷氨酰胺或氨的含量也无变化。在幼鼠大脑中可检测到高浓度的β-N-草酰-L-α,β-二氨基丙酸，而成年动物大脑中则未检测到。结论是β-N-草酰-L-α,β-二氨基丙酸干扰大脑中氨的生成或固定机制，导致慢性氨中毒。
