Brain and retinal damage from lathyrus excitotoxin, β-N-oxalyl-L-α,β-diaminopropionic acid

Abstract

HUMAN consumption of lathyrus peas, especially during periods of famine, has long been associated in certain parts of the world with outbreaks of neurolathyrism, a crippling neurological disorder characterised by spastic paraplegia¹. A neuroexcitatory² amino acid, β-N-oxalyl-L-α,β-diaminopropionic acid (ODAP), isolated from the seeds of Lathyrus sativus³ is suspected to be the responsible neurotoxic principle. Although paralysis of the lower extremities has been reported in adult monkeys after lumbar intrathecal administration of ODAP⁴, and similar symptoms have been induced in newborn chicks by intraperitoneal administration³, evidence for central nervous tissue damage from systemically administered ODAP has been lacking. We now report that ODAP, administered intraperitoneally to immature mice, induces lesions in the retina, hypothalamus and lower medulla. This pattern of damage is similar to that demonstrated in animals after oral or subcutaneous administration of glutamate (Glu).