Co-occurrence of beta-N-methylamino-L-alanine, a neurotoxic amino acid with other cyanobacterial toxins in British waterbodies, 1990-2004.
ABSTRACT The neurotoxic amino acid, beta-N-methylamino-L-alanine, was found to be present in all of 12 analysed samples of cyanobacterial blooms, scums and mats, which had been collected in seven years between 1990 and 2004 inclusive and stored at -20 degrees C. BMAA identification was by high performance liquid chromatography with fluorescence detection and by triple quadrapole mass spectrometry after derivatization. The samples originated from 11 freshwater lakes and 1 brackish waterbody, used either for drinking water, recreation, or both. BMAA was present at between 8 and 287 microg g(-1) cyanobacterial dry weight and was present as both the free amino acid and associated with precipitated proteins. Ten of the samples contained additional cyanotoxins (including microcystins, anatoxin-a, nodularin and saxitoxin) at the time of sample collection. Five of the samples were associated with animal deaths, attributable at the time of sample collection, to microcystins, nodularin or anatoxin-a. The data demonstrate the presence of BMAA by high performance liquid chromatography and mass spectrometry in a diverse range of cyanobacterial bloom samples from high resource waterbodies. Furthermore, samples collected over several years shows that BMAA can co-occur with other known cyanotoxins in such waterbodies. Health risk assessment of cyanobacterial BMAA in waterbodies is suggested.
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ABSTRACT: The occurrence of harmful cyanobacterial blooms in surface waters is often accompanied by a production of a variety of cyanotoxins that are generally classified according to the organs on which they act: hepatotoxins (liver), neurotoxins (nervous system) and dermatotoxins (skin). The presence of such toxins has been reported throughout the world and it appears that liver-toxic microcystins are more commonly found in 50-75 % cyanobacterial blooms. The contamination of surface water by these cyanotoxins can cause water quality problems for fisheries, aquaculture, farming, and sanitary hazard for human and animals. Humans may be exposed to cyanobacterial toxins via several routes, including drinking water, recreational contact, some cyanobacteria-based dietary supplements, and food chain. Information on exposure through aquatic food webs, which is generally scarce, is urgently needed and must not be ignored because aquatic organisms could in a direct or indirect manner contribute to food chain cyanotoxin's transfer, and by the way constitute a potent health risk source.Zooplankton and Phytoplankton : Types, characteristics and ecology, Edited by Giri Kattel, 01/2011: chapter 1: pages 1-34; Nova Science Publishers, Inc., New York., ISBN: ISBN 978-1-61324-508-8
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ABSTRACT: β-N-Methylamino-l-alanine (BMAA), a neurotoxic non-protein amino acid, plays a significant role as an environmental risk factor in neurodegenerative diseases, such as amyotrophic lateral sclerosis. BMAA producers occur globally, colonizing almost all habitats and represent species from distinct phytoplanktonic groups, i.e., cyanobacteria, diatoms, and dinoflagellates. Bioaccumulation of BMAA in invertebrate and vertebrate organisms has also been registered around the globe. In the Baltic Sea, BMAA has been detected in several commercial fish species, raising the question of the bioaccumulation of BMAA in Swedish limnic systems. Here we find the presence of BMAA in water samples from Lake Finjasjön and identify its bioaccumulation patterns in both plankti-benthivorous and piscivorous fish, according to fish species, total weight, gender, and season of collection. For the first time, a large number of fish individuals were used in order to draw conclusions on BMAA bioaccumulation in a closed ecological community based on a statistical approach. We may, therefore, conclude that feeding patterns (plankti-benthivorous) and increased age of fish may lead to a higher tissue concentration of BMAA.Marine Drugs 01/2015; 13(3):1185-201. DOI:10.3390/md13031185 · 3.51 Impact Factor
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ABSTRACT: A cluster of amyotrophic lateral sclerosis (ALS) has been previously described to border Lake Mascoma in Enfield, NH, with an incidence of ALS approximating 25 times expected. We hypothesize a possible association with cyanobacterial blooms that can produce β-N-methylamino-L-alanine (BMAA), a neurotoxic amino acid implicated as a possible cause of ALS/PDC in Guam. Muscle, liver, and brain tissue samples from a Lake Mascoma carp, as well as filtered aerosol samples, were analyzed for microcystins (MC), free and protein-bound BMAA, and the BMAA isomers 2,4-diaminobutyric acid (DAB) and N-(2-aminoethyl)glycine (AEG). In carp brain, BMAA and DAB concentrations were 0.043 μg/g ± 0.02 SD and 0.01 μg/g ± 0.002 SD respectively. In carp liver and muscle, the BMAA concentrations were 1.28 μg/g and 1.27 μg/g respectively, and DAB was not OPEN ACCESS Toxins 2015, 7 323 detected. BMAA was detected in the air filters, as were the isomers DAB and AEG. These results demonstrate that a putative cause for ALS, BMAA, exists in an environment that has a documented cluster of ALS. Although cause and effect have not been demonstrated, our observations and measurements strengthen the association.Toxins 01/2015; 7(2):322-336. DOI:10.3390/toxins7020322 · 2.48 Impact Factor