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      Comparison of the Toxic Effects of Quinolinic Acid and 3-Nitropropionic Acid in C. elegans: Involvement of the SKN-1 Pathway.

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          Abstract

          The tryptophan metabolite, quinolinic acid (QUIN), and the mitochondrial toxin 3-nitropropionic acid (3-NP) are two important tools for toxicological research commonly used in neurotoxic models of excitotoxicity, oxidative stress, energy depletion, and neuronal cell death in mammals. However, their toxic properties have yet to be explored in the nematode Caenorhabditis elegans (C. elegans) for the establishment of novel, simpler, complementary, alternative, and predictive neurotoxic model of mammalian neurotoxicity. In this work, the effects of QUIN (1-100 mM) and 3-NP (1-10 mM) were evaluated on various physiological parameters (survival, locomotion, and longevity) in a wild-type (WT) strand of C. elegans (N2). Their effects were also tested in the VC1772 strain (knock out for the antioxidant SKN-1 pathway) and the VP596 strain (worms with a reporter gene for glutathione S-transferase (GST) transcription) in order to establish the role of the SKN-1 pathway in the mode of action of QUIN and 3-NP. In N2, the higher doses of both toxins decreased survival, though only QUIN altered motor activity. Both toxins also reduced longevity in the VC1772 strain (as compared to N2 strain) and augmented GST transcription in the VP596 strain at the highest doses. The changes induced by both toxins require high doses, and therefore appear moderate when compared with other toxic agents. Nevertheless, the alterations produced by QUIN and 3-NP in C. elegans are relevant to mammalian neurotoxicity as they provide novel mechanistic approaches to the assessment of neurotoxic events comprising oxidative stress and excitotoxicity, in the nematode model.

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          Author and article information

          Journal
          Neurotox Res
          Neurotoxicity research
          Springer Nature
          1476-3524
          1029-8428
          Feb 2018
          : 33
          : 2
          Affiliations
          [1 ] Laboratorio de Aminoácidos Excitadores, Instituto Nacional de Neurología y Neurocirugía, Insurgentes Sur 3877, 14269, Ciudad de México, Mexico.
          [2 ] Facultad de Ciencias, Universidad Nacional Autónoma de México, 04510, Mexico City, Mexico.
          [3 ] Universidade Federal do Pampa, Uruguaiana, RS, Brazil.
          [4 ] Laboratorio de Bacteriología, Facultad de Medicina, Universidad Nacional Autónoma de México, 04510, Mexico City, Mexico.
          [5 ] Laboratorio de Patología Experimental, Instituto Nacional de Neurología y Neurocirugía, 14269, Mexico City, Mexico.
          [6 ] Departamento de Bioquimica e Biologia Molecular, CCNE, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.
          [7 ] Albert Einstein College of Medicine, Jack and Pearl Resnick Campus, Bronx, NY, 10461, USA.
          [8 ] Laboratorio de Aminoácidos Excitadores, Instituto Nacional de Neurología y Neurocirugía, Insurgentes Sur 3877, 14269, Ciudad de México, Mexico. absada@yahoo.com.
          Article
          10.1007/s12640-017-9794-x
          10.1007/s12640-017-9794-x
          28822104
          643cf136-dfe8-41b5-ac1a-95af9bdf75f1
          History

          Excitotoxicity,Huntington’s disease,NMDA,SKN-1,VC1772,VP596
          Excitotoxicity, Huntington’s disease, NMDA, SKN-1, VC1772, VP596

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