Evidence map›Paper›PMID 20421342›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2010

Methylmercury induces acute oxidative stress, altering Nrf2 protein level in primary microglial cells.

Mingwei Ni, Xin Li, Zhaobao Yin, Haiyan Jiang, Marta Sidoryk-Wegrzynowicz, Dejan Milatovic, Jiyang Cai, Michael Aschner

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.

  1. Pooled it
  2. 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
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
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  9. Article
  10. Review
  11. Neuroligin-1 Is a Mediator of Methylmercury Neuromuscular Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2021
    Article
  12. Article
  13. Article
  14. Review
  15. Article
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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

8 authors at 2 institutions in 1 country.

Mingwei NiDepartment of Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA.
Xin Li
Zhaobao Yin
Haiyan Jiang
Marta Sidoryk-Wegrzynowicz
Dejan Milatovic
Jiyang Cai
Michael Aschner
Pediatrics and Genetics · USVanderbilt University Medical Center · US

Funding

Mitochondrial Oxidative Stress and Protection in Pesticide-induced NeurotoxicityR21ES014668 · NIEHS · VANDERBILT UNIVERSITY · PI CAI, JIYANG · 2007 to 2008
$403k
Mitochondrial DNA Variations and Susceptibility to Oxidative Injury in the RPER21EY018715 · NEI · VANDERBILT UNIVERSITY · PI CAI, JIYANG · 2008 to 2009
$402k
PHS HHS 10563
6 · The paper itself

Abstract

The neurotoxicity of methylmercury (MeHg) is well documented in both humans and animals. MeHg causes acute and chronic damage to multiple organs, most profoundly the central nervous system (CNS). Microglial cells are derived from macrophage cell lineage, making up approximately 12% of cells in the CNS, yet their role in MeHg-induced neurotoxicity is not well defined. The purpose of the present study was to characterize microglial vulnerability to MeHg and their potential adaptive response to acute MeHg exposure. We examined the effects of MeHg on microglial viability, reactive oxygen species (ROS) generation, glutathione (GSH) level, redox homeostasis, and Nrf2 protein expression. Our data showed that MeHg (1-5 microM) treatment caused a rapid (within 1 min) concentration- and time-dependent increase in ROS generation, accompanied by a statistically significant decrease in the ratio of GSH and its oxidized form glutathione disulfide (GSSG) (GSH:GSSG ratio). MeHg increased the cytosolic Nrf2 protein level within 1 min of exposure, followed by its nuclear translocation after 10 min of treatment. Consistent with the nuclear translocation of Nrf2, quantitative real-time PCR revealed a concentration-dependent increase in the messenger RNA level of Ho-1, Nqo1, and xCT 30 min post MeHg exposure, whereas Nrf2 knockdown greatly reduced the upregulation of these genes. Furthermore, we observed increased microglial death upon Nrf2 knockdown by the small hairpin RNA approach. Taken together, our study has demonstrated that microglial cells are exquisitely sensitive to MeHg and respond rapidly to MeHg by upregulating the Nrf2-mediated antioxidant response.

Indexed as

Amino Acid Transport Systems, AcidicAmino Acid Transport System y+AnimalsCells, CulturedGlutathioneHeme Oxygenase (Decyclizing)Interleukin-6Methylmercury CompoundsMicrogliaNAD(P)H Dehydrogenase (Quinone)NF-E2-Related Factor 2Oxidative StressProtein TransportRatsRats, Sprague-DawleyAmino Acid Transport Systems, AcidicAmino Acid Transport System y+GlutathioneHeme Oxygenase (Decyclizing)Hmox1 protein, ratInterleukin-6Methylmercury CompoundsNAD(P)H Dehydrogenase (Quinone)Nfe2l2 protein, ratNF-E2-Related Factor 2NQO1 protein, ratSlc7a11 protein, rat

Identifiers

PMID20421342
PMCPMC2905400
OpenAlexW2133041720

What OpenQuestion holds

Textmetadata
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.