Evidence map›Paper›PMID 12140745›Full record

ArticleGenes and immunity2002

Biochemical and molecular basis of thimerosal-induced apoptosis in T cells: a major role of mitochondrial pathway.

S Makani, S Gollapudi, L Yel, S Chiplunkar, S Gupta

Abstract read
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In one paragraph

Article in Genes and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 68 citations in OpenAlex.

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  11. Thimerosal exposure and the role of sulfation chemistry and thiol availability in autism.International journal of environmental research and public health · 2013
    Review
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  17. Cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009
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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

5 authors at 1 institution in 1 country.

S MakaniCellular and Molecular Immunology Laboratories, Division of Basic and Clinical Immunology, University of California, Irvine 92697, USA.
S Gollapudi
L Yel
S Chiplunkar
S Gupta
University of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The major source of thimerosal (ethyl mercury thiosalicylate) exposure is childhood vaccines. It is believed that the children are exposed to significant accumulative dosage of thimerosal during the first 2 years of life via immunization. Because of health-related concerns for exposure to mercury, we examined the effects of thimerosal on the biochemical and molecular steps of mitochondrial pathway of apoptosis in Jurkat T cells. Thimerosal and not thiosalcylic acid (non-mercury component of thimerosal), in a concentration-dependent manner, induced apoptosis in T cells as determined by TUNEL and propidium iodide assays, suggesting a role of mercury in T cell apoptosis. Apoptosis was associated with depolarization of mitochondrial membrane, release of cytochrome c and apoptosis inducing factor (AIF) from the mitochondria, and activation of caspase-9 and caspase-3, but not of caspase-8. In addition, thimerosal in a concentration-dependent manner inhibited the expression of XIAP, cIAP-1 but did not influence cIAP-2 expression. Furthermore, thimerosal enhanced intracellular reactive oxygen species and reduced intracellular glutathione (GSH). Finally, exogenous glutathione protected T cells from thimerosal-induced apoptosis by upregulation of XIAP and cIAP1 and by inhibiting activation of both caspase-9 and caspase-3. These data suggest that thimerosal induces apoptosis in T cells via mitochondrial pathway by inducing oxidative stress and depletion of GSH.

Indexed as

ApoptosisApoptosis Inducing FactorCaspase 3Caspase 9CaspasesCytochrome c GroupEnzyme ActivationFlavoproteinsGlutathioneHumansJurkat CellsMembrane PotentialsMembrane ProteinsMitochondriaOxidative StressPreservatives, PharmaceuticalAIFM1 protein, humanApoptosis Inducing FactorCASP3 protein, humanCASP9 protein, humanCaspase 3Caspase 9CaspasesCytochrome c GroupFlavoproteinsGlutathioneMembrane ProteinsPreservatives, PharmaceuticalProteinsReactive Oxygen SpeciesSalicylatesSulfhydryl CompoundsThimerosalthiosalicylic acidXIAP protein, humanX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID12140745
OpenAlexW2057856508

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.