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UPA Perpustakaan Universitas Jember

β-N-Methylamino-L-Alanine Toxicity in PC12: Excitotoxicity vs. Misincorporation

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The implication of β-N-methylamino-L-alanine
(BMAA) in the development of neurodegenerative diseases
worldwide has led to several investigations of the mechanism,
or mechanisms, of toxicity of this cyanobacterially produced
amino acid. The primary mechanism of toxicity that was iden-
tified is excitotoxicity, with a second possible mechanism, the
misincorporation of BMAA into the primary protein structure
and consequent cell damage, having been more recently re-
p o r t e d . H o w e v e r, s t u d i e s o n e x c i t o t o x i c i t y a n d
misincorporation have been conducted independently and
there are therefore no data available on the relative contribu-
tion of each of these mechanisms to the total toxicity of
BMAA. The rat pheochromocytoma cell line PC12 is an ideal
model for a study of this type, as glutamate receptor expres-
sion is modified by cell differentiation, which can be affected
by exposure to nerve growth factor. In this study, the PC12
cell line was evaluated as a model to study BMAA toxicity via
the two proposed mechanisms: excitotoxicity and protein
misincorporation. BMAA and canavanine treatment of

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