Cyanobacterial Neurotoxins: Their Occurrence and Mechanisms of Toxicity

Abstract

Cyanobacteria are some of the oldest organisms on earth, and have evolved to produce a battery of toxic metabolites, including hepatotoxins, dermatoxins, and neurotoxins. In this review, we focus on the occurrence and mechanisms of toxicity of a number of neurotoxins synthesised by these ancient photosynthetic prokaryotes. We discuss the evidence linking β-methylamino-L-alanine (BMAA), a non-protein amino acid, to an unusual neurological disease complex reported on the island of Guam in the 1950s, and how 60 years later, the role that BMAA plays in human disease is still unclear. There is now evidence that BMAA is also produced by some eukaryotes, and can bioaccumulate in food chains; this combined with higher frequency of cyanobacterial blooms globally, increases the potential for human exposure. Three BMAA isomers that often co-occur with BMAA have been identified, and the current knowledge on the toxicity of these molecules is presented. The acute alkaloid toxins; anatoxin-a, homoanatoxin-a and the saxitoxins, and the organophosphate neurotoxin anatoxin-a(S) are also discussed. In many cases, human exposure to a cocktail of cyanobacterial neurotoxins is likely; however, the implications of combined exposure to these toxins have not been fully explored. Increased understanding of the combined effects of cyanobacterial neurotoxins is required to fully understand how these molecules impact on human health.

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