Journal
TOXICON
Volume 60, Issue 6, Pages 1159-1165Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.toxicon.2012.07.169
Keywords
BMAA; Human neurons; Excitotoxicity; ALS/PDC; Neurotoxin; Cyanotoxin
Categories
Funding
- Australian Research Council
- University of New South Wales
- Association pour la Recherche sur la Sclerose amyotrophique laterale (ARS)
- Alzheimer's Australia Viertel Foundation Postdoctoral Research Fellowship at the University of New South Wales
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The toxicity of the cyanobacterial modified amino acid, BMAA, has been described in rat, mouse and leech neurons. Particular emphasis has been placed on the potential ability of BMAA to induce neuronal damage via excitotoxic mechanisms. Here we present data indicating that the effects observed on lower organisms are also evident in a human model. Our data indicates that BMAA induces increased intracellular Ca2+ influx, DNA damage, mitochondrial activity, lactate dehydrogenase (LDH) release and generation of reactive oxygen species (ROS). The amelioration of LDH release in the presence of the N-methyl-D-aspartate (NMDA) receptor antagonist MK801 indicates that the neurotoxic effects of BMAA are mediated via NMDA receptor activation. Additionally, we have shown that BMAA induces the expression of neuronal nitric oxide synthase (nNOS) and caspase-3 indicating that it can stimulate apoptosis in human neurons, presumably via activation of NMDA receptors. Crown Copyright (C) 2012 Published by Elsevier Ltd. All rights reserved.
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