| Literature DB >> 32236898 |
Tao Ke1, Julia Bornhorst2, Tanja Schwerdtle2, Abel Santamaría3, Félix Alexandre Antunes Soare4, João B T Rocha4, Marcelo Farina5, Aaron B Bowman6, Michael Aschner7.
Abstract
Methylmercury (MeHg) is a global pollutant and potent neurotoxin. In humans, MeHg damages the central nervous system (CNS), causing irreversible neuronal shrinkage, and neuronal loss. Most chelators for clinical mercury detoxification are thiol-containing agents. N,N 'bis-(2-mercaptoethyl) isophthalamide (NBMI) is a lipophilic thiol agent synthesized from natural chemicals. NBMI has high affinity for mercury, cadmium and lead, and can decrease their concentrations in polluted water. However, the efficacy of NBMI for MeHg toxicity has yet to be evaluated in intact animals. Here we used the nematode Caenorhabditis elegans (C. elegans) to test the efficacy of NBMI in attenuating MeHg toxicity in vivo in the whole organism. The results showed that NBMI reduced both the acute toxicity (125 μM MeHg, 1 h) and chronic (5 μM MeHg, 24 h) MeHg toxicity. Co-treatment with NBMI achieved maximal efficacy against MeHg toxicity, however delayed treatment 6 days after initiation of exposure was also effective at reducing neurotoxicity. Co-treatment of NBMI reduced the worms' death rate, structural damage in DAergic neurons, and restored antioxidant response levels. While this study provides proof of principle for the therapeutic value of NBMI in MeHg toxicity, future studies are needed to address the cellular and molecular mechanisms and translatability of these effects to humans and other animals.Entities:
Keywords: Chelation; DAergic neuron; Methylmercury; Oxidative stress
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Year: 2020 PMID: 32236898 PMCID: PMC7924665 DOI: 10.1007/s12640-020-00194-0
Source DB: PubMed Journal: Neurotox Res ISSN: 1029-8428 Impact factor: 3.911