Evidence map›Paper›PMID 24530425›Full record

ArticleDevelopmental biology2014

Prenatal exposure to chromium induces early reproductive senescence by increasing germ cell apoptosis and advancing germ cell cyst breakdown in the F1 offspring.

Kirthiram K Sivakumar, Jone A Stanley, Joe A Arosh, Melissa E Pepling, Robert C Burghardt, Sakhila K Banu

Abstract read
In one paragraph

Article in Developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.3field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 50 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Kirthiram K SivakumarDepartment of Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, TAMU-4458, Texas A&M University, College Station, TX 77843, USA.
Jone A StanleyDepartment of Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, TAMU-4458, Texas A&M University, College Station, TX 77843, USA.
Joe A AroshDepartment of Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, TAMU-4458, Texas A&M University, College Station, TX 77843, USA.
Melissa E PeplingDepartment of Biology, Syracuse University, 114 Life Sciences Complex, 107 College Place, Syracuse, NY 13244, USA.
Robert C BurghardtDepartment of Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, TAMU-4458, Texas A&M University, College Station, TX 77843, USA.
Sakhila K BanuDepartment of Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, TAMU-4458, Texas A&M University, College Station, TX 77843, USA. Electronic address: skbanu@cvm.tamu.edu.
Texas A&M University · USSyracuse University · US

Funding

Chromium VI-induced toxicity on Female Reproductive FunctionR21ES020561 · NIEHS · TEXAS A&M UNIVERSITY · PI BANU, SAKHILA · 2011 to 2012
$403k
NIEHS NIH HHS ES020561-01NIEHS NIH HHS R21 ES020561
6 · The paper itself

Abstract

Hexavalent chromium (CrVI), one of the more toxic heavy metals, is widely used in more than 50 industries such as chrome plating, welding, wood processing and tanneries. As one of the world's leading producers of chromium compounds, the U.S. is facing growing challenges in protecting human health against multiple adverse effects of CrVI. CrVI is rapidly converted to CrIII intracellularly, and can induce apoptosis through different mechanisms. Our previous studies demonstrated postnatal exposure to CrVI results in a delay or arrest in follicle development and puberty. Pregnant rats were treated with 25 ppm potassium dichromate (CrVI) from gestational day (GD) 9.5 to 14.5 through drinking water, placentae were removed on GD 20, and total Cr was estimated in the placentae; ovaries were removed from the F1 offspring on postnatal day (PND)-1 and various analyses were performed. Our results show that gestational exposure to CrVI resulted in (i) increased Cr concentration in the placenta, (ii) increased germ cell apoptosis by up-regulating p53/p27-Bax-caspase-3 proteins and by increasing p53-SOD-2 co-localization; (iii) accelerated germ cell cyst (GCC) breakdown; (iv) advanced primordial follicle assembly and primary follicle transition and (v) down regulation of p-AKT, p-ERK and XIAP. As a result of the above events, CrVI induced early reproductive senescence and decrease in litter size in F1 female progeny.

Indexed as

ApoptosisAnimalsChromiumCystsFemaleGene Expression RegulationGerm CellsImmunohistochemistryMaternal ExposureMicroscopy, FluorescenceOvarian FollicleOvaryPlacentaPotassium DichromatePregnancyPregnancy, AnimalChromiumchromium hexavalent ionPotassium DichromateTumor Suppressor Protein p53ChromiumFollicle atresiaGerm cell cyst breakdownOvaryPrimordial follicle

Identifiers

PMID24530425
PMCPMC3991725
OpenAlexW1989988635

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.