The toxic secondary metabolites β-N-methylamino-L-alanine (BMAA) and 2,4-diaminobutyric acid (DAB) produced by phytoplankton groups such as cyanobacteria, diatoms and dinoflagellates are known to cause neurotoxicity in vertebrates. BMAA has been linked to development of the neurodegenerative diseases amyotrophic lateral sclerosis/Parkinsonism dementia complex (ALS/PDC) and Alzheimer's disease. Despite these risks, previous studies have focused mostly on food webs in aquatic ecosystems as a possible source of human exposure to BMAA and DAB. Moreover, most studies in regard to the producer of BMAA and DAB are biased towards cyanobacteria.

The first aim of this thesis was to investigate the possible risk of human exposure to BMAA via the agro-aqua cycle that artificially interconnects agriculture and aquaculture. Two groups of commercial chickens, fed on either standard feed or standard feed mixed with blue mussel meat, were investigated. The results show that BMAA can be transferred to and accumulated in the chickens through the mixed fodder. It has been suggested that the consumption of chicken may cause a risk of human exposure to BMAA if the chickens are fed with the fodder mixed with mussel meat (Paper I).

The second aim was to assess the effect of biotic stresses (i.e. predation, competition) as possible causative factors to regulate the production of BMAA and/or DAB in diatoms, and assess the toxic effect of BMAA and/or DAB on predator and competitor (if specific production patterns occur for either toxin). The production of DAB was specially regulated only in the diatom T. pseudonana as responses to the predation and the competition. The toxic effect of DAB was significant on the population growth of the copepod Tigriopus sp. as predator, and the growth of cell numbers in T. pseudonana as competitor. However, given the environmental relevance of the DAB effect, the results suggest that DAB may play an important role in the defense mechanisms of the diatom T. pseudonana (Paper II and III).

The last aim was to study the effect and function of BMAA in the diatom Phaeodactylum tricornutum. P. tricornutum was exposed to different concentrations of BMAA. The results showed concentration dependent responses to BMAA. The following were observed when the growth (i.e. cell number) of P. tricornutum was arrested due to exogenous BMAA; oxidative stress, reduced carbon fixation, increase in intracellular Chl a, alterations in GS-GOGAT, and suppressed urea cycle. The results suggest that BMAA represents a toxic secondary metabolite capable of controlling the growth of P. tricornutum via oxidative stress and alterations in the activity of photosynthesis and nitrogen metabolism (Paper IV).