Detection and potential biomagnification of the neurotoxin β-methylamino-L-alanine (BMAA) and its isomers in Western Lake Erie

Harmful algal blooms (HABs) release toxic compounds in water and are increasing in frequency worldwide due to eutrophication. HABs in Lake Erie are monitored extensively, but the neurotoxin β-methylamino-L-alanine (BMAA) has not been fully characterized in this system. Our objectives were to determine the presence of BMAA and its isomers, N-(2-aminoethyl) glycine (AEG), 2,4-diaminobutyric acid (DAB), and β-amino-N-methylalanine (BAMA), in Lake Erie organisms and the possibility of toxin biomagnification. We sampled zooplankton, mussels, forage fish, adult yellow perch, and adult walleye near Point Pelee, Ontario, Canada, and quantified their trophic positions. BMAA and its isomers were quantified using liquid chromatography with tandem mass spectrometry in zooplankton, mussels, and fish samples, and trophic position was quantified using nitrogen stable isotope analysis in whole invertebrate samples and fish muscle tissue. BMAA was detected in 26% of samples tested, while AEG, DAB, and BAMA were detected in 90.6%, 48%, and 71.3% of the samples, respectively. AEG, DAB and BAMA were detected in zooplankton, mussels, and fish. BMAA was detected in brains of forage fish and yellow perch but not walleye, zooplankton or mussels. Isomer concentrations varied across adult fish tissues, and species differences were also observed in the brain. A positive relationship between trophic position and brain DAB concentration provided some support for toxin biomagnification in this food web. However, the relationship was not maintained when considering only fish, highlighting that the evidence of DAB biomagnification is not strong. Our findings show that isomers of BMAA may represent a greater risk to aquatic wildlife than BMAA itself and raise questions about organismal exposure route and metabolism of these toxins.