Evidence map›Paper›PMID 30659883›Full record

ReviewBiochimica et biophysica acta. General subjects2019

Glutathione antioxidant system and methylmercury-induced neurotoxicity: An intriguing interplay.

Marcelo Farina, Michael Aschner

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta. General subjects, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
8.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Seasonal impact on the thermal tolerance window of a keystone coastal grazer, the common periwinkle Littorina littorea.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Intestinal microbiota protects against methylmercury-induced neurotoxicity.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. The Role of the Thioredoxin System in Brain Diseases.Antioxidants (Basel, Switzerland) · 2022
    Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Marcelo FarinaDepartamento de Bioquímica, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Florianópolis, SC, Brazil. Electronic address: marcelo.farina@ufsc.br.
Michael AschnerDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, New York, USA.
Albert Einstein College of Medicine · USUniversidade Federal de Santa Catarina · BR

Funding

Mechanisms of Manganese NeurotoxicityR01ES010563 · NIEHS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Michael Aschner, Aaron B Bowman · 2001 to 2026
$11.9M
Mechanisms of Methylmercury Induced Neuron ToxicityR01ES007331 · NIEHS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Michael Aschner, Aaron B Bowman · 1996 to 2026
$10.6M
Genetic Modulation of MeHg-Induced Oxidative Stress in the Developing BrainR01ES020852 · NIEHS · VANDERBILT UNIVERSITY · PI ASCHNER, MICHAEL · 2012 to 2016
$1.8M
NIEHS NIH HHS R01 ES007331NIEHS NIH HHS R01 ES010563NIEHS NIH HHS R01 ES020852
6 · The paper itself

Abstract

Methylmercury (MeHg) is a toxic chemical compound naturally produced mainly in the aquatic environment through the methylation of inorganic mercury catalyzed by aquatic microorganisms. MeHg is biomagnified in the aquatic food chain and, consequently, piscivorous fish at the top of the food chain possess huge amounts of MeHg (at the ppm level). Some populations that have fish as main protein's source can be exposed to exceedingly high levels of MeHg and develop signs of toxicity. MeHg is toxic to several organs, but the central nervous system (CNS) represents a preferential target, especially during development (prenatal and early postnatal periods). Though the biochemical events involved in MeHg-(neuro)toxicity are not yet entirely comprehended, a vast literature indicates that its pro-oxidative properties explain, at least partially, several of its neurotoxic effects. As result of its electrophilicity, MeHg interacts with (and oxidize) nucleophilic groups, such as thiols and selenols, present in proteins or low-molecular weight molecules. It is noteworthy that such interactions modify the redox state of these groups and, therefore, lead to oxidative stress and impaired function of several molecules, culminating in neurotoxicity. Among these molecules, glutathione (GSH; a major thiol antioxidant) and thiol- or selenol-containing enzymes belonging to the GSH antioxidant system represent key molecular targets involved in MeHg-neurotoxicity. In this review, we firstly present a general overview concerning the neurotoxicity of MeHg. Then, we present fundamental aspects of the GSH-antioxidant system, as well as the effects of MeHg on this system.

Indexed as

Methylmercury CompoundsNeurotoxicity SyndromesNeurotoxinsAnimalsAntioxidantsGlutathioneHumansOxidative StressAntioxidantsGlutathioneMethylmercury CompoundsNeurotoxinsAntioxidant systemGlutathioneMethylmercuryNeurotoxicitySelenolsThiols

Identifiers

PMID30659883
PMCPMC6635095
OpenAlexW2910631504

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.