The neurotoxic non-protein amino acid beta-N-methylamino-l-alanine (BMAA) is connected to the development of neurodegenerative diseases. BMAA has been shown to accumulate in aquatic ecosystems, and filter-feeding molluscs seem particularly susceptible to BMAA accumulation. The blue mussels farmed along the Swedish coastline in the Baltic Sea are, due to their small size, exclusively used to produce feed for chicken and fish in the agro-aqua cycle. We have investigated the possible biotransfer of BMAA from mussels, via mussel-based feed, into chickens. Chickens were divided into two groups, the control and the treatment. BMAA was extracted from the muscle, liver, brain, and eye tissues in both chicken groups; a UPLC-MS/MS method was subsequently used to quantify BMAA. The results indicate detectable concentrations of BMAA in both chicken groups. However, the BMAA concentration in chicken was 5.65 times higher in the treatment group than the control group, with the highest concentration found in muscle tissue extracted from the treatment group chickens. These data suggest that there is a BMAA transfer route within the agro-aqua cycle, so further investigation is recommended before using mussel-based feed in the chicken industry.

The neurotoxin β-N-methylamino-L-alanine (BMAA) is an environmental factor connected to neurodegenerative diseases. BMAA can be produced by various microorganisms (e.g. bacteria, cyanobacteria, dinoflagellates and diatoms) present in diverse ecosystems. No previous study has revealed the function of BMAA in diatoms. In the present study, we combined physiological data with metabolomic and transcriptional data in order to investigate the effect and function of BMAA in the diatom Phaeodactylum tricornutum. P. tricornutum, exposed to different concentrations of exogenous BMAA, showed concentration dependent responses. When the concentration of supplemented BMAA was sufficient to arrest the growth of P. tricornutum, oxidative stress and obstructed carbon fixation were obtained from the specific metabolite and transcriptional data. Results also indicated increased concentration of intracellular chlorophyll a and alterations in the GS-GOGAT cycle, whereas the urea cycle was suppressed. We therefore conclude that BMAA represents a toxic metabolite able to control the growth of P. tricornutum by triggering oxidative stress, and further influencing photosynthesis and nitrogen metabolisms.

The neurotoxic secondary metabolite β-N-methylamino-L-alanine (BMAA) and its structural isomer 2,4-diaminobutyric acid (DAB) are known to be produced by various phytoplankton groups. Despite the worldwide spread of these toxin producers, no obvious role and function of BMAA and DAB in diatoms have been identified. Here, we investigated the effects of biotic factors, i.e., predators and competitors, as possible causes of BMAA and/or DAB regulation in the two diatom species Phaeodactylum tricornutum and Thalassiosira pseudonana. DAB was specifically regulated in T. pseudonana by the presence of predators and competitors. The effects of DAB on both diatoms as competitors and on the copepod Tigriopus sp. as predator at individual and at population levels were examined. The toxic effects of DAB on the growth of T. pseudonana and the population of Tigriopus sp. were significant. The effect of DAB as a defensive secondary metabolite is assumed to be environmentally relevant depending on the number of the copepods. The results show a potential function of DAB that can play an important role in defense mechanisms of T. pseudonana.