Abstract
β-Methylamino-l-alanine (BMAA) is a non-proteinogenic amino acid that induces long-term cognitive deficits, as well as an increased neurodegeneration and intracellular fibril formation in the hippocampus of adult rodents following short-time neonatal exposure and in vervet monkey brain following long-term exposure. It has also been proposed to be involved in the etiology of neurodegenerative disease in humans. The aim of this study was to identify metabolic effects not related to excitotoxicity or oxidative stress in human neuroblastoma SH-SY5Y cells. The effects of BMAA (50, 250, 1000 µM) for 24 h on cells differentiated with retinoic acid were studied. Samples were analyzed using LC–MS and NMR spectroscopy to detect altered intracellular polar metabolites. The analysis performed, followed by multivariate pattern recognition techniques, revealed significant perturbations in protein biosynthesis, amino acid metabolism pathways and citrate cycle. Of specific interest were the BMAA-induced alterations in alanine, aspartate and glutamate metabolism and as well as alterations in various neurotransmitters/neuromodulators such as GABA and taurine. The results indicate that BMAA can interfere with metabolic pathways involved in neurotransmission in human neuroblastoma cells.
Highlights
Introduction βMethylamino-l-alanine (BMAA) is a neurotoxic non-proteinogenic amino acid produced by ubiquitous organisms such as cyanobacteria, diatoms and dinoflagellates in terrestrial, marine, brackish and fresh water environments (Jiang et al 2014; O’Neil et al 2012; Paerl and Paul 2012)
Seven days after treatment with retinoic acid the SH-SY5Y cells had differentiated into a neuron-like phenotype and exhibited characteristic morphology including extensive
This filtering procedure retained 1168 features in positive ionization and 1593 features based on data acquired in Multivariate modeling with Principal component analysis (PCA) illustrates the complexity of biological variance observed in the data based on different passages of cells (Fig. 4)
Summary
Introduction βMethylamino-l-alanine (BMAA) is a neurotoxic non-proteinogenic amino acid produced by ubiquitous organisms such as cyanobacteria, diatoms and dinoflagellates in terrestrial, marine, brackish and fresh water environments (Jiang et al 2014; O’Neil et al 2012; Paerl and Paul 2012). It has potential to biomagnify in a terrestrial food chain, and to bioaccumulate in fish and shellfish (Jiang et al 2014). This amino acid is considered as a potential health risk because of its putative role in neurodegenerative diseases (Banack and Cox 2003). BMAA is a developmental neurotoxin inducing long-term cognitive deficits as well as neurodegeneration, astrogliosis, and intracellular fibril formation in the hippocampus of adult rodents following neonatal exposure to BMAA (Karlsson et al 2009b, 2014).
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