Evidence map›Paper›PMID 32905263›Full record

ArticleToxicology research2020

Genome-wide analysis of DNA methylation in testis of male rat exposed to chlorpyrifos.

Linlin Sai, Qiang Jia, Yecui Zhang, Ru Han, Xiao Geng, Gongchang Yu, Shumin Li, Hua Shao, Yuxin Zheng, Cheng Peng

Open access · bronzeAbstract read
In one paragraph

Article in Toxicology research, 2020. 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
0.5field-weighted citation impact, top 37% 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.

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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

10 authors at 3 institutions in 2 countries.

Linlin SaiDepartment of Toxicology, Public Health College, Qingdao University, 308 Ningxia Road, Shinan District Qingdao, Shandong 266071, China.
Qiang JiaDepartment of Toxicology, Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, 18877 Jingshi Road, Lixia District, Ji'nan, Shandong 250062, China.
Yecui ZhangDepartment of Toxicology, Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, 18877 Jingshi Road, Lixia District, Ji'nan, Shandong 250062, China.
Ru HanDepartment of Toxicology, Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, 18877 Jingshi Road, Lixia District, Ji'nan, Shandong 250062, China.
Xiao GengDepartment of Toxicology, Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, 18877 Jingshi Road, Lixia District, Ji'nan, Shandong 250062, China.
Gongchang YuDepartment of Toxicology, Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, 18877 Jingshi Road, Lixia District, Ji'nan, Shandong 250062, China.
Shumin LiDepartment of Toxicology, Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, 18877 Jingshi Road, Lixia District, Ji'nan, Shandong 250062, China.
Hua ShaoDepartment of Toxicology, Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, 18877 Jingshi Road, Lixia District, Ji'nan, Shandong 250062, China.
Yuxin ZhengDepartment of Toxicology, Public Health College, Qingdao University, 308 Ningxia Road, Shinan District Qingdao, Shandong 266071, China.
Cheng PengQueensland Alliance for Environmental Health Sciences (QAEHS), The University of Queensland 20 Cornwall Street, Woolloongabba, QLD 4102, Australia.
Shandong First Medical University · CNQingdao University · CNUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In our previous study, we found that subchronic exposure of chlorpyrifos (CPF) can cause reproductive damage in male rats. However, the mechanisms underlying the reproductive effects of CPF are not well understood. DNA methylation is essential for epigenetic gene regulation in development and disease. Therefore, we aim to compare DNA methylation profiles between controls and CPF-treated rats in order to identify the epigenetic mechanism of male reproductive toxicity induced by CPF. Methylated DNA immunoprecipitation with high-throughput sequencing (MeDIP-seq) was used to investigate the genome-wide DNA methylation pattern in testes of control and CPF-treated rats for 90 days. We identified 27 019 differentially methylated regions (DMRs) (14 150 upmethylated and 12 869 downmethylated) between CPF-exposed and control groups. The DMR-related genes are mainly involved in 113 pathways predicted by Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. The result showed that high methylation gene PIK3CD may play a key role in epigenetic regulation of multiple pathways, such as Ras signaling pathway, AGE-RAGE signaling pathway in diabetic complications, HIF-1 signaling pathway, VEGF signaling pathway, and glioma and Fc epsilon RI signaling pathway in rats exposed to CPF. Our study provides significant explanations for the epigenetic mechanism of male reproductive toxicology induced by CPF.

Indexed as

epigeneticMeDIP-seqorganic damageorganophosphate pesticiderat

Identifiers

PMID32905263
PMCPMC7467273
OpenAlexW3047438853

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.