Evidence map›Paper›PMID 21262251›Full record

ArticleToxicology and applied pharmacology2011

Hexavalent chromium-induced apoptosis of granulosa cells involves selective sub-cellular translocation of Bcl-2 members, ERK1/2 and p53.

Sakhila K Banu, Jone A Stanley, Jehoon Lee, Sam D Stephen, Joe A Arosh, Patricia B Hoyer, Robert C Burghardt

Open access · greenAbstract read
In one paragraph

Article 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 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.2field-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

28 citing papers in PubMed, 81 citations in OpenAlex.

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  12. Sexually Dimorphic Impact of Chromium Accumulation on Human Placental Oxidative Stress and Apoptosis.Toxicological sciences : an official journal of the Society of Toxicology · 2018
    Article
  13. CoQ10 Deficiency May Indicate Mitochondrial Dysfunction in Cr(VI) Toxicity.International journal of molecular sciences · 2017
    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

7 authors at 2 institutions in 1 country.

Sakhila K BanuDepartment of Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843, USA. skbanu@cvm.tamu.edu
Jone A Stanley
Jehoon Lee
Sam D Stephen
Joe A Arosh
Patricia B Hoyer
Robert C Burghardt
Texas A&M University · USUniversity of Arizona · US

Funding

Mechanism of Prenatal Chromium-VI Exposure and Germ Cell Apoptosis in the OvaryR01ES025234 · NIEHS · TEXAS A&M AGRILIFE RESEARCH · PI BANU, SAKHILA · 2016 to 2020
$1.7M
Chromium VI-induced toxicity on Female Reproductive FunctionR21ES020561 · NIEHS · TEXAS A&M UNIVERSITY · PI BANU, SAKHILA · 2011 to 2012
$403k
Effects of Lactational Exposure to Chromium (VI) on Ovarian DevelopmentR03ES016605 · NIEHS · TEXAS A&M UNIVERSITY · PI BANU, SAKHILA · 2009 to 2010
$146k
NIEHS NIH HHS ES016605-01A2NIEHS NIH HHS R01 ES025234NIEHS NIH HHS R03 ES016605NIEHS NIH HHS R21 ES020561
6 · The paper itself

Abstract

Hexavalent chromium (CrVI) has been widely used in industries throughout the world. Increased usage of CrVI and atmospheric emission of CrVI from catalytic converters of automobiles, and its improper disposal causes various health hazards including female infertility. Recently we have reported that lactational exposure to CrVI induced a delay/arrest in follicular development at the secondary follicular stage. In order to investigate the underlying mechanism, primary cultures of rat granulosa cells were treated with 10 μM potassium dichromate (CrVI) for 12 and 24h, with or without vitamin C pre-treatment for 24h. The effects of CrVI on intrinsic apoptotic pathway(s) were investigated. Our data indicated that CrVI: (i) induced DNA fragmentation and increased apoptosis, (ii) increased cytochrome c release from the mitochondria to cytosol, (iii) downregulated anti-apoptotic Bcl-2, Bcl-XL, HSP70 and HSP90; upregulated pro-apoptotic BAX and BAD, (iv) altered translocation of Bcl-2, Bcl-XL, BAX, BAD, HSP70 and HSP90 to the mitochondria, (v) upregulated p-ERK and p-JNK, and selectively translocated p-ERK to the mitochondria and nucleus, (vi) activated caspase-3 and PARP, and (vii) increased phosphorylation of p53 at ser-6, ser-9, ser-15, ser-20, ser-37, ser-46 and ser-392, increased p53 transcriptional activation, and downregulated MDM-2. Vitamin C pre-treatment mitigated CrVI effects on apoptosis and related pathways. Our study, for the first time provides a clear insight into the effect of CrVI on multiple pathways that lead to apoptosis of granulosa cells which could be mitigated by vitamin C.

Indexed as

AnimalsAntioxidantsApoptosisAscorbic AcidChromiumDNA FragmentationDown-RegulationFemaleGranulosa CellsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-bcl-2RatsRats, Sprague-DawleyTumor Suppressor Protein p53Up-RegulationAntioxidantsAscorbic AcidChromiumchromium hexavalent ionMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-bcl-2Tumor Suppressor Protein p53

Identifiers

PMID21262251
PMCPMC3131794
OpenAlexW1976477577

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.