Abstract
The neurotoxin β-N-methylamino-l-alanine (BMAA) has been identified as an environmental factor triggering neurodegenerative diseases such as Amyotrophic Lateral Sclerosis (ALS) and Alzheimer’s disease (AD). We investigated the possible vectors of BMAA and its isomers 2,4-diaminobutyric acid (DAB) and N-2(aminoethyl)glycine (AEG) in marine mollusks collected from the Chinese coast. Sixty-eight samples of marine mollusks were collected along the Chinese coast in 2016, and were analyzed by an HILIC-MS/MS (hydrophilic interaction liquid chromatography with tandem quadrupole mass spectrometer) method without derivatization. BMAA was detected in a total of five samples from three species: Neverita didyma, Solen strictus, and Mytilus coruscus. The top three concentrations of free-form BMAA (0.99~3.97 μg·g−1 wet weight) were detected in N. didyma. DAB was universally detected in most of the mollusk samples (53/68) with no species-specific or regional differences (0.051~2.65 μg·g−1 wet weight). No AEG was detected in any mollusk samples tested here. The results indicate that the gastropod N. didyma might be an important vector of the neurotoxin BMAA in the Chinese marine ecosystem. The neurotoxin DAB was universally present in marine bivalve and gastropod mollusks. Since N. didyma is consumed by humans, we suggest that the origin and risk of BMAA and DAB toxins in the marine ecosystem should be further investigated in the future.
Highlights
BMAA (β-N-methylamino-L-alanine), as an unusual amino acid, has been hypothesized to trigger the pathogenesis of neurodegenerative diseases like Amyotrophic Lateral Sclerosis (ALS)and Alzheimer’s disease (AD) [1,2]
diaminobutyric acid (DAB) was detected in 78% of the samples (53/68) representing 23 species in this was detected in aconcentrations total of five samples from three species collected from Chinese research
Weremarine detected in the same species of benthic was detected in a total of five samples from three marine species collected from Chinese coastal waters
Summary
BMAA (β-N-methylamino-L-alanine), as an unusual amino acid, has been hypothesized to trigger the pathogenesis of neurodegenerative diseases like Amyotrophic Lateral Sclerosis (ALS)and Alzheimer’s disease (AD) [1,2]. BMAA (β-N-methylamino-L-alanine), as an unusual amino acid, has been hypothesized to trigger the pathogenesis of neurodegenerative diseases like Amyotrophic Lateral Sclerosis (ALS). Extensive in vitro experiments have demonstrated that the neurotoxicity of BMAA for neurons is a result of multiple mechanisms including action at NMDA (N-methyl-D-aspartic acid) or AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid)/kainate receptors, generation of ROS (reactive oxygen species), and production of excessive dopamine [3,4,5,6,7]. The accumulation of BMAA in zooplankton results in a loss of swimming ability, phototaxis, and reproductive ability, which may be linked to toxicity due to oxidative. Mar. Drugs 2016, 14, 202; doi:10.3390/md14110202 www.mdpi.com/journal/marinedrugs. Mar. Drugs 2016, 14, 202 stress [10,11,12]. Neuro-muscular and developmental abnormalities of zebrafish (Danio rerio) embryos
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