Literature DB >> 28889277

Neurodegeneration Induced by Metals in Caenorhabditis elegans.

Felix Antunes Soares1, Daiandra Almeida Fagundez2, Daiana Silva Avila3.   

Abstract

Metals are a component of a variety of ecosystems and organisms. They can generally be divided into essential and nonessential metals. The essential metals are involved in physiological processes once the deficiency of these metals has been associated with diseases. Although iron, manganese, copper, and zinc are important for life, it has been evidenced that they are also involved in neuronal damage in many neurodegenerative disorders. Nonessential metals, which are metals without physiological functions, are present in trace or higher levels in living organisms. Occupational, environmental, or deliberate exposures to lead, mercury, aluminum, and cadmium are clearly correlated with the increase of toxicity and varied kinds of pathological situations. Actually, the field of neurotoxicology needs to satisfy two opposing demands: the testing of a growing list of chemicals and resource limitations and ethical concerns associated with testing using traditional mammalian species. Toxicological assays using alternative animal models may relieve some of this pressure by allowing testing of more compounds while reducing expenses and using fewer mammals. The nervous system is by far the more complex system in C. elegans. Almost a third of their cells are neurons (302 neurons versus 959 cells in adult hermaphrodite). It initially underwent extensive development as a model organism in order to study the nervous system, and its neuronal lineage and the complete wiring diagram of its nervous system are stereotyped and fully described. The neurotransmission systems are phylogenetically conserved from nematodes to vertebrates, which allows for findings from C. elegans to be extrapolated and further confirmed in vertebrate systems. Different strains of C. elegans offer a new perspective on neurodegenerative processes. Some genes have been found to be related to neurodegeneration induced by metals. Studying these interactions may be an effective tool to slow neuronal loss and deterioration.

Entities:  

Keywords:  Aluminum; Cadmium; Copper; Iron; Lead; Manganese; Mercury; Neurodegenerative diseases; Zinc

Mesh:

Substances:

Year:  2017        PMID: 28889277     DOI: 10.1007/978-3-319-60189-2_18

Source DB:  PubMed          Journal:  Adv Neurobiol


  4 in total

1.  Application of Fluorescence Microscopy and Behavioral Assays to Demonstrating Neuronal Connectomes and Neurotransmitter Systems in C. elegans.

Authors:  Omamuyovwi M Ijomone; Priscila Gubert; Comfort O A Okoh; Alexandre M Varão; Leandro de O Amara; Oritoke M Aluko; Michael Aschner
Journal:  Neuromethods       Date:  2021-07-24

2.  Glial loss of the metallo β-lactamase domain containing protein, SWIP-10, induces age- and glutamate-signaling dependent, dopamine neuron degeneration.

Authors:  Chelsea L Gibson; Joseph T Balbona; Ashlin Niedzwiecki; Peter Rodriguez; Ken C Q Nguyen; David H Hall; Randy D Blakely
Journal:  PLoS Genet       Date:  2018-03-28       Impact factor: 5.917

3.  Iron overload and neurodegenerative diseases: What can we learn from Caenorhabditis elegans?

Authors:  Airton C Martins; Miriam B Virgolini; Alexey A Tinkov; Anatoly V Skalny; Rohan P Tirumala; Marcelo Farina; Abel Santamaria; Rongzhu Lu; Michael Aschner
Journal:  Toxicol Res Appl       Date:  2022-04-23

Review 4.  The intertwining between lead and ethanol in the model organism Caenorhabditis elegans.

Authors:  P A Albrecht; L E Fernandez-Hubeid; R Deza-Ponzio; M B Virgolini
Journal:  Front Toxicol       Date:  2022-09-20
  4 in total

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