The fate of the cyanobacterial toxin β-N-methylamino-L-alanine in freshwater mussels

Ecotoxicol Environ Saf. 2014 Mar:101:51-8. doi: 10.1016/j.ecoenv.2013.11.028. Epub 2014 Jan 11.

Abstract

The cyanobacterial neurotoxin, β-N-methylamino-l-alanine (BMAA) has been suggested as a causative agent for certain neurodegenerative diseases. This cyanotoxin bioaccumulates in an array of aquatic organisms, in which it occurs as both a free amino acid and in a protein-associated form. This study was intended to investigate the environmental fate of BMAA by examining the metabolism of isotopically labeled BMAA in four freshwater mussel species. All species showed substantial uptake of BMAA from the culture media. Data showed no significant evidence for BMAA catabolism in any of the animals but did suggest metabolism via the reversible covalent modification of BMAA in freshwater mussels, a process that appears to be variable in different species.

Keywords: BMAA; Cyanobacteria; Metabolism; Mussels; Neurotoxin; β-N-methylamino-l-alanine.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acids, Diamino / metabolism*
  • Animals
  • Bacterial Toxins / metabolism*
  • Bivalvia / chemistry*
  • Bivalvia / metabolism*
  • Cyanobacteria Toxins
  • Fresh Water*
  • Marine Toxins / metabolism*
  • Microcystins / metabolism*
  • Water Pollutants, Chemical / metabolism*

Substances

  • Amino Acids, Diamino
  • Bacterial Toxins
  • Cyanobacteria Toxins
  • Marine Toxins
  • Microcystins
  • Water Pollutants, Chemical
  • beta-N-methylamino-L-alanine