β-N-methylamino-L-alanine (BMAA) metabolism in the aquatic macrophyte Ceratophyllum demersum

• The cyanobacterial neurotoxin β-N-methylamino-L-alanine is not catabolised by Cerratophyllum demersum.
• β-N-methylamino-L-alanine is covalently modified in Cerratophyllum demersum.
• β-N-methylamino-L-alanine appears to sequestered inside the plant as a BMAA derivative.

The cyanobacterial neurotoxin, β-N-methylamino-l-alanine (BMAA) bioaccumulates and biomagnifies within the environment. However, most reports on the environmental presence of BMAA focus on the presence of BMAA in animals rather than in plants. Various laboratory studies have reported that this neurotoxin, implicated in neurodegenerative disease, is rapidly taken up by various aquatic and terrestrial plants, including crop plants. In this study the metabolism of BMAA in the aquatic macrophyte, Ceratophyllum demersum, was investigated using stable isotopically labelled BMAA. Data show that the toxin is rapidly removed from the environment by the plant. However, during depuration cellular BMAA concentrations decrease considerably, without excretion of the toxin back into the environment and without catabolism of BMAA, evidenced by the absence of label transfer to other amino acids. This strongly suggests that BMAA is metabolised via covalent modification and sequestered inside the plant as a BMAA-derivative. This modification may be reversed in humans following consumption of BMAA-containing plant material. These data therefore impact on the assessment of the risk of human exposure to this neurotoxin.