Evidence map›Paper›PMID 28881573›Full record

ArticleOncotarget2017

Histopathological findings of renal tissue induced by oxidative stress due to different concentrations of fluoride.

Qin Luo, Hengmin Cui, Huidan Deng, Ping Kuang, Huan Liu, Yujiao Lu, Jing Fang, Zhicai Zuo, Junliang Deng, Yinglun Li and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.4field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Mononuclear Aluminum-Fluoride Ions, AlFMolecules (Basel, Switzerland) · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Copper Induces Oxidative Stress and Apoptosis in the Mouse Liver.Oxidative medicine and cellular longevity · 2020
    Article
  8. Selenium attenuates apoptosis and p-AMPK expressions in fluoride-induced NRK-52E cells.Environmental science and pollution research international · 2019
    Article
  9. Review
  10. Article
  11. A mini review of fluoride-induced apoptotic pathways.Environmental science and pollution research international · 2018
    Review
  12. Article
  13. Article
  14. 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

12 authors at 1 institution in 1 country.

Qin LuoCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, China.
Hengmin CuiCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, China.
Huidan DengCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, China.
Ping KuangCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, China.
Huan LiuCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, China.
Yujiao LuCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, China.
Jing FangCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, China.
Zhicai ZuoCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, China.
Junliang DengCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, China.
Yinglun LiCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, China.
Xun WangCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, China.
Ling ZhaoCollege of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, China.
Sichuan Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been reported that excessive intake of fluoride can induce renal lesions. However, its pathogenesis is still less understood. Therefore, this study was conducted to investigate oxidative damage and the relationships between the oxidative damage and renal lesions in fluoride-treated mice by using the methods of histopathology, biochemistry, flow cytometry and quantitative real-time polymerase chain reaction (qRT-PCR). A total of 240 ICR mice were randomly divided into four equal groups (sodium fluoride was given orally at the dose of 0, 12, 24 and 48 mg/kg body weight for 42 days, respectively). We found that fluoride in excess of 12 mg/kg induced renal oxidative damage, which was characterized by increasing the levels of reactive oxygen species (ROS) production and contents of malondialdehyde (MDA) and protein carbonyls (PC), and decreasing the abilities of anti-superoxide anion (ASA) and anti-hydroxyl radical (AHR), glutathione (GSH) content, as well as activities and mRNA expression levels of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione peroxidase (GSH-Px). Concurrently, fluoride caused degeneration and necrosis of the tubular cells, renal tubular hyaline casts and glomeruli swelling, which were consistent with the alteration of renal function parameters including elevated contents of serum creatinine (Cr), serum uric acid (UA), blood urea nitrogen (BUN), and the activities of urinary N-acetyl-b-D-glucosaminidase (NAG), renal lactate dehydrogenase (LDH), and reduced activities of sodium-potassium adenosine triphosphatase (Na+/K+-ATPase) and acid phosphatase (ACP) in the kidney. The above-mentioned results showed that fluoride in excess of 12 mg/kg induced renal oxidative damage, which then caused renal lesions and dysfunctions. These findings also clearly demonstrated that oxidative damage is one of the mechanisms of fluoride-induced renal lesions and dysfunctions.

Indexed as

dysfunctionImmune responseImmunityImmunology and Microbiology Sectionkidneylesionoxidative damagesodium fluoride

Identifiers

PMID28881573
PMCPMC5584147
OpenAlexW2606399203

What OpenQuestion holds

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LicenceCC BY
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.