Co-occurrence of β-N-methylamino-L-alanine, a neurotoxic amino acid with other cyanobacterial toxins in British waterbodies, 1990-2004. Environ Microbiol
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.
- SourceAvailable from: Lothar Krienitz
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- "an archive of cyanobacterial bloom, scum and mat samples from UK fresh-and brackish waterbodies showed that BMAA can co-occur with microcystins, anatoxin-a and saxitoxins, in addition to the probably invariable production of lipopolysaccharide (LPS) endotoxins by the cyanobacteria and other associated bacteria in these environments (Metcalf et al., 2008). Little is known about the ecotoxicological significance of the co-production of multiple classes of cyanotoxins although research indicates that exposure to combinations of cyanotoxins and the timing of exposure to the individual cyanotoxins can affect toxicological outcomes in aquatic biota (Best et al., 2002; Lindsay et al., 2006). "
ABSTRACT: The Lesser Flamingo (Phoeniconaias minor) is known to use cyanobacteria (primarily Arthrospira) as a major food source in the East African Rift Valley lakes. Periodically, mass mortalities have occurred, associated with the cyanobacterial toxins (cyanotoxins), microcystins and anatoxin-a. Deposition of these cyanotoxins into P. minor feathers has been shown to occur, consistent with the presence of cyanotoxins in the livers, stomach and faecal contents after dietary intake. As cyanobacteria have been shown to also produce the neurotoxins β-N-methylamino-l-alanine (BMAA) and 2,4-diaminobutyric acid (DAB), stored wing feathers, previously recovered from flamingos which had been exposed to microcystins and anatoxin-a and had subsequently died, were analysed for these neurotoxic amino acids. Trace amounts of BMAA were detected in extracts from Lake Nakuru flamingo feathers, with DAB also present at concentrations between 3.5 and 8.5μgg(-1) dry weight in feathers from both lakes. Toxin recovery by solid-phase extraction of feather digests was tested with spiked deuterated BMAA and showed good recovery when analysed by LC-MS/MS (80-94%). This is the first report of these neurotoxic amino acids in birds. We discuss the origin and significance of DAB, alongside other cyanotoxins of dietary origin, in the feathers of the Lesser Flamingo.Chemosphere 10/2012; 90(2). DOI:10.1016/j.chemosphere.2012.09.094 · 3.50 Impact Factor
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- "Recent reports have indicated that most cyanobacteria can produce the neurotoxic nonprotein amino acid β-N-methylamino-l-alanine (BMAA) (Banack et al., 2007; Cox et al., 2005). Cyanobacteria are ubiquitous microorganisms capable of massive increase in numbers (algal blooming) in various types of waters all over the world, and BMAA has been detected in several water systems including temperate aquatic ecosystems (Caller et al., 2009; Esterhuizen and Downing, 2008; Metcalf et al., 2008). Recreational water activity is a primary cause of cyanotoxin exposure in addition to contaminated food and drinking water (Freeman, 2010; Valerio et al., 2010). "
ABSTRACT: The cyanobacterial toxin β-N-methylamino-L-alanine (BMAA) has been proposed to contribute to neurodegenerative disease. We have previously reported a selective uptake of BMAA in the mouse neonatal hippocampus and that exposure during the neonatal period causes learning and memory impairments in adult rats. The aim of this study was to characterize effects in the brain of six month-old rats treated neonatally (postnatal days 9-10) with the glutamatergic BMAA. Protein changes were examined using the novel technique Matrix Assisted Laser Desorption Ionization (MALDI) imaging mass spectrometry (IMS) for direct imaging of proteins in brain cryosections, and histological changes were examined using immunohistochemistry and histopathology. The results showed long-term changes including a decreased expression of proteins involved in energy metabolism and intracellular signalling in the adult hippocampus at a dose (150 mg/kg) that gave no histopathological lesions in this brain region. Developmental exposure to a higher dose (460 mg/kg) also induced changes in the expression of S100β, histones, calcium and calmodulin-binding proteins and guanine nucleotide-binding proteins. At this dose, severe lesions in the adult hippocampus including neuronal degeneration, cell loss, calcium deposits and astrogliosis were evident. The data demonstrate subtle, sometimes dose-dependent, but permanent effects of a low neonatal dose of BMAA in the adult hippocampus suggesting that BMAA could potentially disturb many processes during the development. The detection of BMAA in seafood stresses the importance of evaluating the magnitude of human exposure to this neurotoxin.Toxicological Sciences 08/2012; 130(2). DOI:10.1093/toxsci/kfs241 · 4.48 Impact Factor
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- "The potential dangers of BMAA acting as an accessory or combinatorial toxin, rather than being highly toxic as a sole entity, were indicated by Lobner et al.  when they demonstrated that BMAA can potentiate the activity of other insults. As BMAA has been shown to be co-present with other cyanotoxins, such as microcystin, anatoxin-a, nodularin and saxitoxin , this potentiation capability, may implicate BMAA as an important factor when considering the management strategies of these other toxins. The debate between BSSG and BMAA appears to be very polarized, with acceptance of one causative agent completely ruling out the significance of the other. "
ABSTRACT: The association of α-amino-β-methylaminopropionic acid (BMAA) with elevated incidence of amyotrophic lateral sclerosis/Parkinson's disease complex (ALS/PDC) was first identified on the island of Guam. BMAA has been shown to be produced across the cyanobacterial order and its detection has been reported in a variety of aquatic and terrestrial environments worldwide, suggesting that it is ubiquitous. Various in vivo studies on rats, mice, chicks and monkeys have shown that it can cause neurodegenerative symptoms such as ataxia and convulsions. Zebrafish research has also shown disruption to neural development after BMAA exposure. In vitro studies on mice, rats and leeches have shown that BMAA acts predominantly on motor neurons. Observed increases in the generation of reactive oxygen species (ROS) and Ca(2+) influx, coupled with disruption to mitochondrial activity and general neuronal death, indicate that the main mode of activity is via excitotoxic mechanisms. The current review pertaining to the neurotoxicity of BMAA clearly demonstrates its ability to adversely affect neural tissues, and implicates it as a potentially significant compound in the aetiology of neurodegenerative disease. When considering the potential adverse health effects upon exposure to this compound, further research to better understand the modes of toxicity of BMAA and the environmental exposure limits is essential.International Journal of Environmental Research and Public Health 09/2011; 8(9):3728-46. DOI:10.3390/ijerph8093728 · 2.06 Impact Factor