Evidence map›Paper›PMID 35457433›Full record

ArticleInternational journal of environmental research and public health2022

Flurochloridone Induced Cell Apoptosis via ER Stress and eIF2α-ATF4/ATF6-CHOP-Bim/Bax Signaling Pathways in Mouse TM4 Sertoli Cells.

Fen Zhang, Zhijing Ni, Shuqi Zhao, Yanna Wang, Xiuli Chang, Zhijun Zhou

Open access · goldAbstract read
In one paragraph

Article in International journal of environmental research and public health, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 24% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Endocrine Disrupting Agents: Toxicological Aspects on Male Reproduction.Reproductive sciences (Thousand Oaks, Calif.) · 2025
    Review
  3. Article
  4. Effect ofTranslational cancer research · 2024
    Article
  5. Article
  6. Review
  7. 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.

Fen ZhangSchool of Public Health, MOE Key Laboratory for Public Health Safety/NHC Key Lab of Health Technology Assessment, Fudan University, Shanghai 200032, China.
Zhijing NiSchool of Public Health, MOE Key Laboratory for Public Health Safety/NHC Key Lab of Health Technology Assessment, Fudan University, Shanghai 200032, China.
Shuqi ZhaoSchool of Public Health, MOE Key Laboratory for Public Health Safety/NHC Key Lab of Health Technology Assessment, Fudan University, Shanghai 200032, China.
Yanna WangSchool of Public Health, MOE Key Laboratory for Public Health Safety/NHC Key Lab of Health Technology Assessment, Fudan University, Shanghai 200032, China.
Xiuli ChangSchool of Public Health, MOE Key Laboratory for Public Health Safety/NHC Key Lab of Health Technology Assessment, Fudan University, Shanghai 200032, China.
Zhijun ZhouSchool of Public Health, MOE Key Laboratory for Public Health Safety/NHC Key Lab of Health Technology Assessment, Fudan University, Shanghai 200032, China.ORCID 0000-0002-2407-2071
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Flurochloridone (FLC), as a novel herbicide, has been widely used in many countries since 1980s. Current studies have shown that FLC has toxic effects on male reproduction and its target organ is testis, while the underlying mechanism is still unknown. Mouse testis Sertoli cell line TM4 cells were used as an in vitro model and treated with FLC at different doses (40, 80, 160 μM) for different times (6, 12, 24 h). Cell viability, cytotoxicity and apoptotic cells were detected by CCK-8 assay, LDH leakage assay and flow cytometry. The protein levels of GRP78, phosphorylated-eIF2α, ATF4, ATF6, CHOP, Bim and Bax were observed by Western Blot and Immunofluorescence staining. FLC inhibited cell viability and induced cytotoxicity in dose-dependent way in TM4 cells. The percentage of apoptotic cells were 6.2% ± 0.6%, 7.3% ± 0.3%, 9.8% ± 0.4%, 13.2% ± 0.2%, respectively. The expression levels of ER stress and UPR related proteins were activated over dose. Meanwhile, the pro-apoptotic proteins (Bim and Bax) were also up-regulated in dose-dependent. After pretreated with ISRIB, the inhibitor of eIF2α phosphorylation, the elevated expression of GRP78, phosphorylated-eIF2α, ATF4, ATF6, CHOP and Bim was down to normal level accordingly. In conclusion, FLC induced apoptosis in TM4 cells mediated by UPR signaling pathways.

Indexed as

Endoplasmic Reticulum StressEukaryotic Initiation Factor-2PyrrolidinonesActivating Transcription Factor 6AnimalsApoptosisbcl-2-Associated X ProteinMaleMiceSertoli CellsSignal TransductionActivating Transcription Factor 6Atf6 protein, mousebcl-2-Associated X ProteinEukaryotic Initiation Factor-2Pyrrolidinonesraiserapoptosisendoplasmic reticulum stressFlurochloridonetesticular toxicityTM4 Sertoli cellsunfolded protein response

Identifiers

PMID35457433
PMCPMC9024663
OpenAlexW4223429412

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.