Evidence map›Paper›PMID 26355036›Full record

ArticleScientific reports2015

Hexavalent chromium induces apoptosis in male somatic and spermatogonial stem cells via redox imbalance.

Joydeep Das, Min-Hee Kang, Eunsu Kim, Deug-Nam Kwon, Yun-Jung Choi, Jin-Hoi Kim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Endocrine Disrupting Agents: Toxicological Aspects on Male Reproduction.Reproductive sciences (Thousand Oaks, Calif.) · 2025
    Review
  5. Article
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  7. Article
  8. Article
  9. Review
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  11. Article
  12. Unsafe herbal sex enhancement supplements in Nigerian markets: a human risk assessment.Environmental science and pollution research international · 2019
    Article
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  14. Article
  15. 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

6 authors at 1 institution in 1 country.

Joydeep DasDepartment of Animal Biotechnology, College of Animal Bioscience and Biotechnology/Animal Resources Research Center, Konkuk University, Seoul 143-701, South Korea.
Min-Hee KangDepartment of Animal Biotechnology, College of Animal Bioscience and Biotechnology/Animal Resources Research Center, Konkuk University, Seoul 143-701, South Korea.
Eunsu KimDepartment of Animal Biotechnology, College of Animal Bioscience and Biotechnology/Animal Resources Research Center, Konkuk University, Seoul 143-701, South Korea.
Deug-Nam KwonDepartment of Animal Biotechnology, College of Animal Bioscience and Biotechnology/Animal Resources Research Center, Konkuk University, Seoul 143-701, South Korea.
Yun-Jung ChoiDepartment of Animal Biotechnology, College of Animal Bioscience and Biotechnology/Animal Resources Research Center, Konkuk University, Seoul 143-701, South Korea.
Jin-Hoi KimDepartment of Animal Biotechnology, College of Animal Bioscience and Biotechnology/Animal Resources Research Center, Konkuk University, Seoul 143-701, South Korea.
Konkuk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hexavalent chromium [Cr(VI)], an environmental toxicant, causes severe male reproductive abnormalities. However, the actual mechanisms of toxicity are not clearly understood and have not been studied in detail. The present in vitro study aimed to investigate the mechanism of reproductive toxicity of Cr(VI) in male somatic cells (mouse TM3 Leydig cells and TM4 Sertoli cells) and spermatogonial stem cells (SSCs) because damage to or dysfunction of these cells can directly affect spermatogenesis, resulting in male infertility. Cr(VI) by inducing oxidative stress was cytotoxic to both male somatic cells and SSCs in a dose-dependent manner, and induced mitochondria-dependent apoptosis. Although the mechanism of Cr(VI)-induced cytotoxicity was similar in both somatic cells, the differences in sensitivity of TM3 and TM4 cells to Cr(VI) could be attributed, at least in part, to cell-specific regulation of P-AKT1, P-ERK1/2, and P-P53 proteins. Cr(VI) affected the differentiation and self-renewal mechanisms of SSCs, disrupted steroidogenesis in TM3 cells, while in TM4 cells, the expression of tight junction signaling and cell receptor molecules was affected as well as the secretory functions were impaired. In conclusion, our results show that Cr(VI) is cytotoxic and impairs the physiological functions of male somatic cells and SSCs.

Indexed as

AnimalsApoptosisChromiumGene Expression RegulationGlial Cell Line-Derived Neurotrophic FactorInhibitory Concentration 50MaleMatrix MetalloproteinasesMembrane Potential, MitochondrialMiceMitogen-Activated Protein KinasesModels, BiologicalOxidation-ReductionOxidative StressProto-Oncogene Proteins c-aktReactive Oxygen SpeciesAkt1 protein, mouseChromiumchromium hexavalent ionGlial Cell Line-Derived Neurotrophic FactorMatrix MetalloproteinasesMitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesRNA, MessengerTumor Suppressor Protein p53

Identifiers

PMID26355036
PMCPMC4564811
OpenAlexW2437160591

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.