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O
O
O
H
OH
OH
NH 2
ß-oxalylaminoalanine (BOAA)
NH 2
H
N
OH
H 3 C
O
ß -methylaminoalanine (BMAA)
Fig. 10.6. Neurotoxic, non-protein amino acids from plants
that can inhibit protein synthesis, disrupt urea cycle function or impair
neurotransmission (Bell 2003). One example of a neurologically damaging
aminoacidfromplantsis
β
-oxalylaminoalanine (BOAA) found in Lathyrus
sativus . L. sativus (grasspea or chickling vetch, guaya in Ethiopia, khesari
in India) is a small legume grown and eaten throughout many parts of
the world. Consumption of seeds high in BOAA is thought to be the cause
of lathyrism, a neurodegenerative disease characterized by spastic para-
paresis. Taken in small quantities, pigeonpea is not neurotoxic but during
droughts or when other food is limited, epidemics in lathyrism have oc-
curred (Spencer, 1999). In 1977 an outbreak of lathyrism in Ethiopia caused
more than 2,500 people to become ill (Spencer and Palmer 2003). Both
BOAA and a related compound BMAA (Fig. 10.6) can damage neurons
but the potency and specificity of these amino acids is quite low (Lind-
strom et al. 1990). The compounds are classified as excitotoxins, a toxic
molecule that overstimulates stimulates neurons resulting in cellular dam-
age or cell death. In cell cultures, both BOAA and
β
-methylaminoalanine
(BMAA) injure neurons in a dose-dependent manner and require various
metabolic cofactors such as bicarbonate (Weiss et al. 1989). As a result
of both the general complexity of progressive neurodegenerative diseases
and the mechanisms of action of compounds that are not acutely toxic,
the study of plant-based neurotoxins requires an interdisciplinary team of
neurologists, chemists and botanists. One example of this type of research
is the study of the epidemic of progressive neurodegenerative disease on
Guam.
 
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