Algal toxins are bioactive compounds produced by specific microalgal groups, posing significant risks to human and ecosystem health. Reports of their impact have increased worldwide, which reflects a growing concern and research activity. This review provides a comprehensive analysis of the growth, trends, and topics of algal toxin research, using data from ScienceDirect and Web of Science. Although publications have risen steadily since 2001, fragmentation across databases highlights the need for integrative syntheses. In addition, three representative microalgal neurotoxins – domoic acid (DA), β-N-methylamino-L-alanine (BMAA), and 2,4-diaminobutyric acid (DAB) – are examined with emphasis on how biotic stressors, specifically predation and competition, influence their production and biosynthesis in the causative diatoms. Distinct biotic pressures elicit divergent neurotoxin responses: grazing by herbivorous copepods and copepodamides enhances DA production in Pseudo-nitzschia seriata via activation of the dab gene cluster; competition through physical contact induces BMAA production in Thalassiosira minima, mediated by cysteine synthase; and predation pressure stimulates DAB production in Thalassiosira pseudonana through a separate regulatory pathway. Current predator-competition studies have addressed only a limited subset of possible species interactions, underscoring the need for broader experimental matrices and additional model organisms.

2, 4-diaminobutryic acid (DAB) and its structural isomer β-N-methylamino-L-alanine (BMAA) are environmental agents associated with neurotoxicity. A variety of aquatic microorganisms, including diatoms, have the capability to produce DAB and BMAA. Previous research has demonstrated an increase in DAB production in the diatom Thalassiosira pseudonana as a result of predation. Therefore, in this study, we investigated whether the production of DAB as a defensive metabolite is a species-specific strategy or a general approach employed by diatoms to counter predation. The diatom species Phaeodactylum tricornutum and Chaetoceros socialis, along with the copepod Tigriopus sp. were used for the experiment. The copepod did not consume C. socialis, and no specific regulation of DAB and BMAA productions was observed in any of the diatom species. The findings show that the production of DAB and BMAA does not contribute to the defense mechanisms of the diatom P. tricornutum.

The neurotoxin β-N-methylamino-L-alanine (BMAA) has emerged as an environmental factor related to neurodegenerative diseases. BMAA is produced by various microorganisms including cyanobacteria and diatoms, in diverse ecosystems. In the diatom Phaeodactylum tricornutum, BMAA is known to inhibit growth. The present study investigated the impact of BMAA on the diatom Thalassiosira pseudonana by exposing it to different concentrations of exogenous BMAA. Metabolomics was predominantly employed to investigate the effect of BMAA on T. pseudonana, and MetaboAnalyst (https://www.metabo-analyst.ca/) was used to identify BMAA-associated metabolisms/pathways in T. pseudonana. Furthermore, to explore the unique response, specific metabolites were compared between treatments. When the growth was obstructed by BMAA, 17 metabolisms/pathways including nitrogen and glutathione (i.e. oxidative stress) metabolisms, were influenced in T. pseudonana. This study has further determined that 11 out of 17 metabolisms/pathways could be essentially affected by BMAA, leading to the inhibition of diatom growth.

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.

The neurotoxin β-N-methylamino-L-alanine (BMAA), a non-proteinogenic amino acid produced by several species of both prokaryotic (cyanobacteria) and eukaryotic (diatoms) microorganisms, has been proposed to be associated with the development of neurodegenerative diseases. At first, BMAA appeared to be ubiquitously present worldwide in various organisms, from aquatic and terrestrial food webs. However, recent studies, using detection methods based on mass spectrometry, instead of fluorescence detection, suggest that the trophic transfer of BMAA is debatable. This study evaluated BMAA in 22 cetaceans of three different species (Phocoena phocoena, n = 8, Delphinus delphis, n = 8, and Tursiops truncatus, n = 6), found stranded in North-West Spain. BMAA analysis of the liver, kidney, or muscle tissues via sensitive liquid chromatography with tandem mass spectrometry did not reveal the presence of this compound or its isomers. The absence recorded in this study highlights the need to better understand the trophic transfer of BMAA and its anatomical distribution in marine mammals.

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 neurotoxins beta-N-methylamino-L-alanine (BMAA) and 2,4-diaminobutyric acid (DAB) are produced by cyanobacteria, diatoms and dinoflagellates and have been detected in seafood worldwide. Our present knowledge of their metabolism or biosynthesis is limited. In this study, the production of BMAA and DAB as a function of time was monitored in five strains representing four species of diatoms, i.e. Phaeodactylum tricornutum, Thalassiosira weissflogii, Thalassiosira pseudonana and Navicula pelliculosa, previously identified as BMAA and DAB producers. Subsequently, three strains were selected and exposed to three nitrogen treatments - starvation, control (the standard concentration in f/2 medium) and enrichment, because BMAA metabolism has been suggested to be closely associated with cellular nitrogen metabolism in both cyanobacteria and diatoms. Chlorophyll a and total protein concentrations were also determined. Our results indicate that BMAA and DAB production in diatoms is species- and strain-specific. However, production might also be affected by stress, particularly as related to nitrogen starvation and cell density. Furthermore, this study shows a significant correlation between the production of the two neurotoxins which might further suggest common steps in the metabolic pathways.

The native Ruditapes decussatus and the non-indigenous Ruditapes philippinarum are an important target of shellfish industries. The aim of this study was to compare an invader with a native species living in sympatry in the view of marine biotoxins accumulation. Samples were analysed for regulated and non regulated biotoxins. The consistently occurrence of okadaic acid-group toxins and BMAA, may cause human health problems and economical losses. A strong positive relationship was observed between species, with significantly higher DSP toxicity in R. decussatus. Similar toxin profiles dominated by DTX3 in both species suggests similar metabolic pathways. Lower DSP toxicity in R. philippinarum may favour their cultivation, but a tendency for higher levels of the non-regulated BMAA was observed, indicating risks for consumers that are not monitored. This study highlights the need to better understand the physiological responses and adaptations allowing similar species exposed to the same conditions to present different toxicity levels.

beta-N-Methylamino-l-alanine (BMAA), a neurotoxin reportedly produced by cyanobacteria, diatoms and dinoflagellates, is proposed to be linked to the development of neurological diseases. BMAA has been found in aquatic and terrestrial ecosystems worldwide, both in its phytoplankton producers and in several invertebrate and vertebrate organisms that bioaccumulate it. LC-MS/MS is the most frequently used analytical technique in BMAA research due to its high selectivity, though consensus is lacking as to the best extraction method to apply. This study accordingly surveys the efficiency of three extraction methods regularly used in BMAA research to extract BMAA from cyanobacteria samples. The results obtained provide insights into possible reasons for the BMAA concentration discrepancies in previous publications. In addition and according to the method validation guidelines for analysing cyanotoxins, the TCA protein precipitation method, followed by AQC derivatization and LC-MS/MS analysis, is now validated for extracting protein-bound (after protein hydrolysis) and free BMAA from cyanobacteria matrix. BMAA biological variability was also tested through the extraction of diatom and cyanobacteria species, revealing a high variance in BMAA levels (0.0080-2.5797 mu g g(-1) DW).