Ubiquity of the neurotoxin β-N-methylamino-L-alanine and its isomers confirmed by two different mass spectrometric methods in diverse marine mollusks

Li, Aifeng; Hu, Yang; Song, Jialiang; Wang, Shuqin; Deng, Longji

doi:10.1016/j.toxicon.2018.07.004

Cited by 19 publications

(7 citation statements)

References 44 publications

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“…Since analysis of the BMAA isomer BAMA began ca. 2012, earlier studies using mass spectrometry may have failed to obtain adequate selectivity of BMAA over its isomers (Jiang et al 2012;Beach et al 2015Beach et al , 2018Réveillon et al 2015Réveillon et al , 2016Foss et al 2018;Li et al 2018). We note that BMAA and BAMA are widely separated by retention times using AQC derivatization (Banack 2020).…”

Section: Planktonmentioning

confidence: 76%

“…We note that BMAA and BAMA are widely separated by retention times using AQC derivatization (Banack 2020). The m/z transition 119 > 102 in underivatized methods has shown inconsistent results in the literature (Baker et al 2018;Beach et al 2018;Li et al 2018;Tymm et al 2019). Authors have used additional ion separation steps, such as differential mobility spectrometry (DMS), which acts as an ion filter by separating ions in a matrix based on their mobility in high or low electrical field strength, to adequately separate BMAA from BAMA but this requires a skilled analyst (Beach et al 2015(Beach et al , 2018.…”

Section: Planktonmentioning

confidence: 81%

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Is Exposure to BMAA a Risk Factor for Neurodegenerative Diseases? A Response to a Critical Review of the BMAA Hypothesis

Dunlop

et al. 2021

Neurotox Res

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In a literature survey, Chernoff et al. (2017) dismissed the hypothesis that chronic exposure to β-N-methylamino-L-alanine (BMAA) may be a risk factor for progressive neurodegenerative disease. They question the growing scientific literature that suggests the following: (1) BMAA exposure causes ALS/PDC among the indigenous Chamorro people of Guam; (2) Guamanian ALS/PDC shares clinical and neuropathological features with Alzheimer’s disease, Parkinson’s disease, and ALS; (3) one possible mechanism for protein misfolds is misincorporation of BMAA into proteins as a substitute for L-serine; and (4) chronic exposure to BMAA through diet or environmental exposures to cyanobacterial blooms can cause neurodegenerative disease. We here identify multiple errors in their critique including the following: (1) their review selectively cites the published literature; (2) the authors reported favorably on HILIC methods of BMAA detection while the literature shows significant matrix effects and peak coelution in HILIC that may prevent detection and quantification of BMAA in cyanobacteria; (3) the authors build alternative arguments to the BMAA hypothesis, rather than explain the published literature which, to date, has been unable to refute the BMAA hypothesis; and (4) the authors erroneously attribute methods to incorrect studies, indicative of a failure to carefully consider all relevant publications. The lack of attention to BMAA research begins with the review’s title which incorrectly refers to BMAA as a “non-essential” amino acid. Research regarding chronic exposure to BMAA as a cause of human neurodegenerative diseases is emerging and requires additional resources, validation, and research. Here, we propose strategies for improvement in the execution and reporting of analytical methods and the need for additional and well-executed inter-lab comparisons for BMAA quantitation. We emphasize the need for optimization and validation of analytical methods to ensure that they are fit-for-purpose. Although there remain gaps in the literature, an increasingly large body of data from multiple independent labs using orthogonal methods provides increasing evidence that chronic exposure to BMAA may be a risk factor for neurological illness.

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Section: Planktonmentioning

confidence: 76%

Section: Planktonmentioning

confidence: 81%

Is Exposure to BMAA a Risk Factor for Neurodegenerative Diseases? A Response to a Critical Review of the BMAA Hypothesis

Dunlop

et al. 2021

Neurotox Res

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“…Muscle, liver, and brain tissue samples of a huge carp from the Lake Mascoma, as well as filtered aerosol samples contained BMAA 23 . Additionally, positive detection of BMAA was reported in mussels and other mollusks in French coasts [24][25][26] , in Sweden 27,28 , as well as in diverse filter-feeding mollusks or benthic gastropod in China 29,30 . Expectedly higher concentrations of BMAA [144˜1836 μg g -1 wet weight (WW)] were detected in fin samples of sharks from South Florida 31 .…”

Section: Introductionmentioning

confidence: 99%

“…Although the presence of BMAA in cyanobacterial samples is consistent across many studies, the quantitation of BMAA in cyanobacterial samples vary widely and reflects different methods on different samples [37][38][39][40][41][42] . Interestingly, no BMAA was detected from cyanobacteria isolated from Chinese freshwater environments using LC-HILIC-MS/MS method 38 , but BMAA was detected in diverse mollusks and gastropod from marine ecosystem in China using the same method 29,30 . A recent review article described marine bivalves as having higher concentrations of BMAA, far more than most fish muscles, but with an exception for shark cartilage, which hinted that the source of BMAA in aquatic ecosystem requires further investigations 43 .…”

Section: Introductionmentioning

confidence: 99%

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Migration and Transformation Behaviors of Neurotoxin BMAA along Food Chains in a Diatom-dominated Marine Ecosystem in China

Wang¹,

Yan²,

Qiu³

et al. 2020

Preprint

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Neurotoxin β-N-methylamino-L-alanine (BMAA) produced by cyanobacteria and microalgae has been concerned by scientists due to its toxicity to human motoneurons. The source and environmental behaviors of BMAA in marine ecosystem are important to understand its risk to human health. Here a diatoms-dominated marine ecosystem in Jiaozhou Bay, China, was investigated for BMAA contamination in phytoplankton, zooplankton, and marine animals, during four seasons in 2019. Results showed that BMAA was migrated and biomagnified along the food chains from phytoplankton to higher trophic organisms, in which the trophic magnification factors (TMF) for zooplankton, bivalve mollusks, carnivorous crustacea and saprophytic gastropod mollusks were approximately 4.58, 30.1, 42.5, and 74.4, respectively. An isomer of BMAA, β-aminomethyl-L-alanine (BAMA), was ubiquitous in phytoplankton samples and its content ratios to BMAA looks gradually decreased with increasing trophic levels. A total of 56 diatom strains (Pseudo-nitzschia spp., Thalassiosira spp., Chaetoceros spp., Planktoniella spp., Minidiscus spp.) were isolated from the Chinese coast and cultured in the laboratory, among which 21 strains produced BMAA mainly presented in the precipitated bound fraction ranging from 0.11 to 3.95 μg g-1 dry weight. BMAA was firstly detected in both Pseudo-nitzschia and Planktoniella genera in this study. Only 2,4-diaminobutyric acid (DAB) but not BMAA or BAMA was detected in seven symbiotic bacteria isolated from the gut of Neverita didyma, which further proves that the benthic vector of BMAA, N. didyma, accumulated BMAA through food chains. These findings demonstrated that the coastal residents have a risk to accumulate BMAA by consumption of seafood products. Significance StatementThe biomagnification of BMAA along food chains was synthetically investigated and discussed in the diatomdominated marine ecosystem. The ubiquity of BAMA, an isomer of BMAA, was confirmed in the phytoplankton samples using the pre-column derivatization method. Results showed that diatoms are the source of BMAA in marine ecosystem because 21 of 56 diatom strains contained this neurotoxin. No BMAA was detected in the isolated bacterial strains from the gut of the typical vector of BMAA,Neverita didyma , which further confirmed that the toxin BMAA was transferred and accumulated along food chains. All these findings improve our understanding for the environmental behavior and risk to human health of the neurotoxin BMAA.

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Recent advancements in LC‐MS based analysis of biotoxins: Present and future challenges

Panda

Dash

Manickam

et al. 2021

Mass Spectrometry Reviews

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There has been a rising concern regarding the harmful impact of biotoxins, source of origin, and the determination of the specific type of toxin. With numerous reports on their extensive spread, biotoxins pose a critical challenge to figure out their parent groups, metabolites, and concentration. In that aspect, liquid chromatography‐mass spectrometry (LC‐MS) based analysis paves the way for its accurate identification and quantification. The biotoxins are ideally categorized as phytotoxins, mycotoxins, shellfish‐toxins, ciguatoxins, cyanotoxins, and bacterial toxins such as tetrodotoxins. Considering the diverse nature of biotoxins, both low‐resolution mass spectrometry (LRMS) and high‐resolution mass spectrometry (HRMS) methods have been implemented for their detection. The sample preparation strategy for complex matrix usually includes “QuEChERS” extraction or solid‐phase extraction coupled with homogenization and centrifugation. For targeted analysis of biotoxins, the LRMS consisting of a tandem mass spectrometer operating in multiple reaction monitoring mode has been widely implemented. With the help of the reference standard, most of the toxins were accurately quantified. At the same time, the suspect screening and nontarget screening approach are facilitated by the HRMS platforms during the absence of reference standards. Significant progress has also been made in sampling device employment, utilizing novel sample preparation strategies, synthesizing toxin standards, employing hybrid MS platforms, and the associated data interpretation. This critical review attempts to elucidate the progress in LC‐MS based analysis in the determination of biotoxins while pointing out major challenges and suggestions for future development.

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Ubiquity of the neurotoxin β-N-methylamino-L-alanine and its isomers confirmed by two different mass spectrometric methods in diverse marine mollusks

Cited by 19 publications

References 44 publications

Is Exposure to BMAA a Risk Factor for Neurodegenerative Diseases? A Response to a Critical Review of the BMAA Hypothesis

Is Exposure to BMAA a Risk Factor for Neurodegenerative Diseases? A Response to a Critical Review of the BMAA Hypothesis

Migration and Transformation Behaviors of Neurotoxin BMAA along Food Chains in a Diatom-dominated Marine Ecosystem in China

Recent advancements in LC‐MS based analysis of biotoxins: Present and future challenges

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