Evidence map›Paper›PMID 29933360›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2018

Lead Induces Genotoxicity via Oxidative Stress and Promoter Methylation of DNA Repair Genes in Human Lymphoblastoid TK6 Cells.

Xiangquan Liu, Jingying Wu, Wenyan Shi, Wenhua Shi, Hekun Liu, Xiaonan Wu

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

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  11. Genotoxic Effects of Lead and Their Impact on the Expression of DNA Repair Genes.International journal of environmental research and public health · 2022
    Review
  12. Article
  13. Epimutational effects of electronic cigarettes.Environmental science and pollution research international · 2021
    Review
  14. Review
  15. Article
  16. Article
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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.

Xiangquan LiuDepartment of Nutrition and Food Safety, School of Public Health, Fujian Medical University, Fuzhou, Fujian, China (mainland).
Jingying WuDepartment of Preventive Medicine, Fuzhou Center for Disease Control and Prevention, Fuzhou, Fujian, China (mainland).
Wenyan ShiDepartment of Clinical Nutrition, Shenzhen Third People's Hospital, Shenzhen, Guangdong, China (mainland).
Wenhua ShiDepartment of Occupational Health, Fuzhou Center for Disease Control and Prevention, Fuzhou, Fujian, China (mainland).
Hekun LiuDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian, China (mainland).
Xiaonan WuDepartment of Nutrition and Food Safety, School of Public Health, Fujian Medical University, Fuzhou, Fujian, China (mainland).
Fujian Medical University · CNShenzhen Third People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Lead (Pb) is a widely used metal in modern industry and is regarded as a health hazard. Although lead-induced genotoxicity has been confirmed, the direct evidence that lead induces genotoxicity in human cells and its related mechanisms has not been fully elucidated. In this study, for the first time, we evaluated the genotoxicity induced by lead in human lymphoblastoid TK6 cells. MATERIAL AND METHODS The TK6 cells were incubated with various concentrations of Pb(Ac)2 for 6 h, 12 h, or 24 h. Cell viability was detected by CCK8 assay. Various biochemical markers were assessed by specific kits. Immunofluorescence assay was used to detect g-H2AX foci formation. The promoter methylation was assessed by methylation-specific PCR. The protein levels were determined by Western blot assay. RESULTS The results showed that after exposure to lead, cell viability was obviously decreased and γ-H2AX foci formation was significantly enhanced in TK6 cells. Moreover, the levels of 8-OHdG, ROS, MDA, and GSSG were increased, while the GSH level and SOD activity were decreased in lead-treated TK6 cells. The activation of the Nrf2-ARE signaling pathway was involved in lead-induced oxidative stress in TK6 cells. Finally, the expressions of DNA repair genes XRCC1, hOGG-1, BRCA1, and XPD were inhibited via enhancing their promoter methylation in TK6 cells after exposure to lead. CONCLUSIONS Taken together, our study provides the first published evidence that lead exposure results in DNA damage via promoting oxidative stress and the promoter methylation of DNA repair genes in human lymphoblastoid TK6 cells.

Indexed as

DNA DamageAntioxidant Response ElementsDNA MethylationDNA RepairHumansLeadLymphocytesNF-E2-Related Factor 2Oxidative StressPromoter Regions, GeneticRNA, MessengerSignal TransductionLeadNFE2L2 protein, humanNF-E2-Related Factor 2RNA, Messenger

Identifiers

PMID29933360
PMCPMC6045917
OpenAlexW2808789289

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.