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However, mining of a pharmacovigilance database recently ranked DMF as the second pharmaceutical most associated with cognitive adverse events. To our best knowledge, the signaling mechanisms underlying its therapeutic and neurotoxic outcomes remain mostly undisclosed. This work thus represents the first-hand assessment of DMF-induced metabolic changes in undifferentiated SH-SY5Y human neuroblastoma cells, through an untargeted metabolomic approach using gas chromatography\u2013mass spectrometry (GC\u2013MS). The endometabolome was analyzed following 24\u00a0h and 96\u00a0h of exposure to two pharmacologically relevant DMF concentrations (0.1 and 10\u00a0\u03bcM). None of these conditions significantly reduced metabolic activity (MTT reduction assay). Our data showed that 24\u00a0h-exposure to DMF at both concentrations tested mainly affected metabolic pathways involved in mitochondrial activity (e.g., citric acid cycle, de novo triacylglycerol biosynthesis), and the synthesis of catecholamines and serotonin by changing the levels of their respective precursors, namely phenylalanine (0.68-fold decrease for 10\u00a0\u03bcM DMF vs vehicle), and tryptophan (1.36-fold increase for 0.1\u00a0\u03bcM DMF vs vehicle). Interestingly, taurine, whose levels can be modulated via Nrf2 signaling (DMF\u2019s primary target), emerged as a key mediator of DMF\u2019s neuronal action, displaying a 3.86-fold increase and 0.27-fold decrease for 10\u00a0\u03bcM DMF at 24\u00a0h and 96\u00a0h, respectively. A 96\u00a0h-exposure to DMF seemed to mainly trigger pathways associated with glucose production (e.g., gluconeogenesis, glucose-alanine cycle, malate-aspartate shuttle), possibly related to the metabolism of DMF into monomethyl fumarate and its further conversion into glucose via activation of the citric acid cycle. Overall, our data contribute to improving the understanding of the events associated with neuronal exposure to DMF.<\/jats:p>","DOI":"10.1007\/s00204-024-03683-9","type":"journal-article","created":{"date-parts":[[2024,2,18]],"date-time":"2024-02-18T04:46:24Z","timestamp":1708231584000},"page":"1151-1161","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Identification of key neuronal mechanisms triggered by dimethyl fumarate in SH-SY5Y human neuroblastoma cells through a metabolomic approach"],"prefix":"10.1007","volume":"98","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4073-2121","authenticated-orcid":false,"given":"Ana Margarida","family":"Ara\u00fajo","sequence":"first","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8090-5720","authenticated-orcid":false,"given":"Sandra I.","family":"Marques","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7395-5700","authenticated-orcid":false,"given":"Paula","family":"Guedes de Pinho","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6650-5285","authenticated-orcid":false,"given":"Helena","family":"Carmo","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3858-3494","authenticated-orcid":false,"given":"F\u00e9lix","family":"Carvalho","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5656-0897","authenticated-orcid":false,"given":"Jo\u00e3o Pedro","family":"Silva","sequence":"additional","affiliation":[]}],"member":"297","published-online":{"date-parts":[[2024,2,18]]},"reference":[{"key":"3683_CR1","doi-asserted-by":"publisher","first-page":"163","DOI":"10.1186\/1742-2094-9-163","volume":"9","author":"P Albrecht","year":"2012","unstructured":"Albrecht P, Bouchachia I, Goebels N, Henke N, Hofstetter HH, Issberner A, Kovacs Z, Lewerenz J, Lisak D, Maher P, Mausberg A-K, Quasthoff K, Zimmermann C, Hartung H-P, Methner A (2012) Effects of dimethyl fumarate on neuroprotection and immunomodulation. 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