Evidence map›Paper›PMID 28007637›Full record

ArticleToxicology letters2017

Reproductive toxicity of linuron following gestational exposure in rats and underlying mechanisms.

Hongwei Ding, Wei Zheng, Hua Han, Xiyin Hu, Binli Hu, Feng Wang, Liyu Su, Hong Li, Yan Li

Abstract read
In one paragraph

Article in Toxicology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. QuantitativeEnvironmental health perspectives · 2020
    Article
  10. Article
  11. Article
  12. Review
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

9 authors at 2 institutions in 2 countries.

Hongwei DingDepartment of Hygiene Toxicology, School of Public Health, Zunyi Medical College, Zunyi, Guizhou, PR China.
Wei ZhengSchool of Health Sciences, Purdue University, West Lafayette, IN, USA.
Hua HanDepartment of Hygiene Toxicology, School of Public Health, Zunyi Medical College, Zunyi, Guizhou, PR China.
Xiyin HuDepartment of Hygiene Toxicology, School of Public Health, Zunyi Medical College, Zunyi, Guizhou, PR China.
Binli HuDepartment of Hygiene Toxicology, School of Public Health, Zunyi Medical College, Zunyi, Guizhou, PR China.
Feng WangDepartment of Hygiene Toxicology, School of Public Health, Zunyi Medical College, Zunyi, Guizhou, PR China.
Liyu SuDepartment of Hygiene Toxicology, School of Public Health, Zunyi Medical College, Zunyi, Guizhou, PR China.
Hong LiDepartment of Hygiene Toxicology, School of Public Health, Zunyi Medical College, Zunyi, Guizhou, PR China.
Yan LiDepartment of Hygiene Toxicology, School of Public Health, Zunyi Medical College, Zunyi, Guizhou, PR China. Electronic address: liyan067321@sina.com.
Zunyi Medical University · CNPurdue University West Lafayette · US

Funding

Choroid Plexus a Target in Metal-Induced NeurotoxicityR01ES008146 · NIEHS · PURDUE UNIVERSITY WEST LAFAYETTE · PI ZHENG, WEI · 1998 to 2014
$5.0M
NIEHS NIH HHS R01 ES008146
6 · The paper itself

Abstract

Linuron is a widely used herbicide in agriculture; its endocrine disruptive toxicity has recently received public attention. This study was designed to examine the developmental toxicity of linuron on the reproductive system of male offspring following maternal exposure. Mother rats received oral gavages of linuron, once daily, at the dose of 0, 50, 100, 150 or 200mg/kg, from gestational day (GD)13 to GD18; gonadal organs from GD20 fetuses were examined. Data indicated that exposed male offspring had a significantly shortened anogenital distance. Pathological examination further revealed a lack of fusion in the urogenital fold in treated fetuses, the damaged seminiferous tubules, and the injured Leydig cell ultrastructure. Analysis of serum testosterone concentrations at postnatal day (PND)2 showed a significant dose-related reduction (about 33.7-58.75%, r=-0.838, p<0.05) as compared to controls. Immunohistochemical results demonstrated a significantly reduced expression of enzymes pertinent to the testosterone production including P450scc, 3β-HSD, and PCNA in Leydig cells (p<0.05). qPCR studies confirmed decreased levels of mRNAs encoding P450scc, 3β-HSD and PCNA (p<0.05). Taken together, these data suggest that maternal exposure to linuron hampers the male gonadal organ development; this appears to be due to linuron's direct action on the production of testosterone in fetal and postnatal offspring.

Indexed as

AnimalsAnimals, NewbornDose-Response Relationship, DrugFemaleGenitalia, MaleHerbicidesLinuronMalePregnancyPrenatal Exposure Delayed EffectsRatsRats, Sprague-DawleyTestosteroneHerbicidesLinuronTestosteroneDevelopmental toxicityFetusLeydig cellsLinuronOffspringReproductive toxicityTestosterone

Identifiers

PMID28007637
PMCPMC5697898
OpenAlexW2565893129

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.