Evidence map›Paper›PMID 21601588›Full record

ReviewToxicology and applied pharmacology2011

Oxidative stress in MeHg-induced neurotoxicity.

Marcelo Farina, Michael Aschner, João B T Rocha

Open access · greenAbstract readReview
In one paragraph

Review in Toxicology and applied pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed, 2 pooled it
18.6field-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

131 citing papers in PubMed, 2 syntheses or guidelines pooled it, 334 citations in OpenAlex.

  1. Pooled it
  2. Mercury Exposure and Heart Rate Variability: a Systematic Review.Current environmental health reports · 2015
    Pooled it
  3. Article
  4. Article
  5. Clarified açaí (Euterpe oleracea Martius) exerts protective effects against methylmercury toxicity in salivary glands and total saliva.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Article
  6. Mercury-induced excitotoxicity in autism spectrum disorder: disruption of glutamatergic homeostasis and the therapeutic role of the selenium-glutathione axis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
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71 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 2 countries.

Marcelo FarinaDepartamento de Bioquímica, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Florianópolis, SC, Brazil. farina@ccb.ufsc.br
Michael Aschner
João B T Rocha
Universidade Federal de Santa Catarina · BRUniversidade Federal de Santa Maria · BRVanderbilt University Medical Center · US

Funding

Mechanisms of Methylmercury Induced Neuron ToxicityR01ES007331 · NIEHS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Michael Aschner, Aaron B Bowman · 1996 to 2026
$10.6M
NIEHS NIH HHS R01 ES007331NIEHS NIH HHS R01 ES07331
6 · The paper itself

Abstract

Methylmercury (MeHg) is an environmental toxicant that leads to long-lasting neurological and developmental deficits in animals and humans. Although the molecular mechanisms mediating MeHg-induced neurotoxicity are not completely understood, several lines of evidence indicate that oxidative stress represents a critical event related to the neurotoxic effects elicited by this toxicant. The objective of this review is to summarize and discuss data from experimental and epidemiological studies that have been important in clarifying the molecular events which mediate MeHg-induced oxidative damage and, consequently, toxicity. Although unanswered questions remain, the electrophilic properties of MeHg and its ability to oxidize thiols have been reported to play decisive roles to the oxidative consequences observed after MeHg exposure. However, a close examination of the relationship between low levels of MeHg necessary to induce oxidative stress and the high amounts of sulfhydryl-containing antioxidants in mammalian cells (e.g., glutathione) have led to the hypothesis that nucleophilic groups with extremely high affinities for MeHg (e.g., selenols) might represent primary targets in MeHg-induced oxidative stress. Indeed, the inhibition of antioxidant selenoproteins during MeHg poisoning in experimental animals has corroborated this hypothesis. The levels of different reactive species (superoxide anion, hydrogen peroxide and nitric oxide) have been reported to be increased in MeHg-exposed systems, and the mechanisms concerning these increments seem to involve a complex sequence of cascading molecular events, such as mitochondrial dysfunction, excitotoxicity, intracellular calcium dyshomeostasis and decreased antioxidant capacity. This review also discusses potential therapeutic strategies to counteract MeHg-induced toxicity and oxidative stress, emphasizing the use of organic selenocompounds, which generally present higher affinity for MeHg when compared to the classically studied agents.

Indexed as

AnimalsAntioxidantsHumansHydrogen PeroxideLipid PeroxidationMethylmercury CompoundsNeuroprotective AgentsNeurotoxicity SyndromesNitric OxideOxidation-ReductionOxidative StressReactive Oxygen SpeciesSuperoxidesAntioxidantsHydrogen PeroxideMethylmercury CompoundsNeuroprotective AgentsNitric OxideReactive Oxygen SpeciesSuperoxides

Identifiers

PMID21601588
PMCPMC3166649
OpenAlexW2065055202

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.