Evidence map›Paper›PMID 35008820›Full record

ArticleInternational journal of molecular sciences2021

Transport and Toxicity of Methylmercury-Cysteine in Cultured BeWo Cells.

Srividya Ganapathy, Elisa R Farrell, Simran Vaghela, Lucy Joshee, Earl G Ford, Olga Uchakina, Robert J McKallip, Jennifer L Barkin, Christy C Bridges

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

3 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

9 authors at 1 institution in 1 country.

Srividya GanapathyDepartment of Biomedical Sciences, Mercer University School of Medicine, Macon, GA 31207, USA.
Elisa R FarrellDepartment of Biomedical Sciences, Mercer University School of Medicine, Macon, GA 31207, USA.ORCID 0000-0003-1221-3778
Simran VaghelaDepartment of Biomedical Sciences, Mercer University School of Medicine, Macon, GA 31207, USA.
Lucy JosheeDepartment of Biomedical Sciences, Mercer University School of Medicine, Macon, GA 31207, USA.
Earl G FordDepartment of Biomedical Sciences, Mercer University School of Medicine, Macon, GA 31207, USA.
Olga UchakinaDepartment of Biomedical Sciences, Mercer University School of Medicine, Macon, GA 31207, USA.
Robert J McKallipDepartment of Biomedical Sciences, Mercer University School of Medicine, Macon, GA 31207, USA.
Jennifer L BarkinDepartment of Community Medicine, Mercer University School of Medicine, Macon, GA 31207, USA.
Christy C BridgesDepartment of Biomedical Sciences, Mercer University School of Medicine, Macon, GA 31207, USA.ORCID 0000-0003-1603-1445
Mercer University · US

Funding

Navicent Health Foundation N/A
6 · The paper itself

Abstract

Mercury is a heavy metal toxicant that is prevalent throughout the environment. Organic forms of mercury, such as methylmercury (MeHg), can cross the placenta and can lead to lasting detrimental effects in the fetus. The toxicological effects of MeHg on the placenta itself have not been clearly defined. Therefore, the purpose of the current study was to assess the transport of MeHg into placental syncytiotrophoblasts and to characterize the mechanisms by which MeHg exerts its toxic effects. Cultured placental syncytiotrophoblasts (BeWo) were used for these studies. The transport of radioactive MeHg was measured to identify potential mechanisms involved in the uptake of this compound. The toxicological effects of MeHg on BeWo cells were determined by assessing visible pathological change, autophagy, mitochondrial viability, and oxidative stress. The findings of this study suggest that MeHg compounds are transported into BeWo cells primarily by sodium-independent amino acid carriers and organic anion transporters. The MeHg altered mitochondrial function and viability, decreased mitophagy and autophagy, and increased oxidative stress. Exposure to higher concentrations of MeHg inhibited the ability of cells to protect against MeHg-induced injury. The findings show that MeHg is directly toxic to syncytiotrophoblasts and may lead to disruptions in the fetal/maternal transfer of nutrients and wastes.

Indexed as

AutophagyBiological TransportBiomarkersCell LineCell ShapeCell SurvivalCysteineGlutathioneHumansLipid PeroxidationMalondialdehydeMethionineMethylmercury CompoundsMitochondriaModels, BiologicalOxidative StressBiomarkersCysteineGlutathioneMalondialdehydeMethionineMethylmercury Compoundsmethylmercury cysteineTritiumautophagymercuryoxidative stressplacentasyncytiotrophoblasttoxicology

Identifiers

PMID35008820
PMCPMC8745507
OpenAlexW4205822388

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.