Evidence map›Paper›PMID 29790047›Full record

ArticleEnvironmental science and pollution research international2018

Ascorbic acid inhibits cadmium-induced disruption of the blood-testis barrier by regulating oxidative stress-mediated p38 MAPK pathways.

Na Chen, Ping Su, Mei Wang, Ya-Min Li

Abstract read
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In one paragraph

Article in Environmental science and pollution research international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Review
  3. Endocrine Disrupting Agents: Toxicological Aspects on Male Reproduction.Reproductive sciences (Thousand Oaks, Calif.) · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Exposure to low-dose cadmium induces testicular ferroptosis.Ecotoxicology and environmental safety · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Na ChenFamily Planning Research Institute, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Ping SuFamily Planning Research Institute, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. Suping5022@163.com.
Mei WangFamily Planning Research Institute, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Ya-Min LiFamily Planning Research Institute, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Huazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ascorbic acid (AA), one of the best-known reactive oxygen species (ROS) scavengers, exhibits numerous functions such as antioxidant, anti-cancer, and anti-inflammatory effects. Increasing evidence demonstrates that oxidative stress plays an important role in testicular toxicity. In the present study, we investigated the protective effect of AA against cadmium (Cd)-induced blood-testis barrier (BTB) disruption. Sprague-Dawley (SD) rats were divided into four groups: the Cd-treated group received a single dose (s.c.) of 2 mg/kg BW cadmium chloride; the AA antagonism group received an injection of AA at a dose of 400 mg/kg BW (200 mg 24 h prior to Cd treatment and 200 mg 24 h following Cd treatment); and the control groups received an equal volume of saline or an equal dose of AA. As expected, ROS expression was upregulated in the Cd-treated rats, accompanied by an increase in malondialdehyde (MDA). Interestingly, AA suppressed Cd-induced oxidative stress by decreasing the levels of ROS and MDA and increasing the activity of superoxide dismutase (SOD) and catalase (CAT). In addition, AA also reduced BTB disruption by inhibiting TGF-β3 activation and p38 MAPK phosphorylation. Significant decreases in occludin and claudin-11 expression were observed in the Cd-treated rats, whereas AA administration attenuated this effect. Moreover, testicular histopathology and transmission electron microscopy further demonstrated the protective effects of AA against Cd-induced BTB damage. In conclusion, the results of the present study suggest that AA protects BTB destruction via the inhibition of oxidative stress and the TGF-β3/p38 MAPK signalling pathway in the testis of Cd-exposed rats.

Indexed as

AnimalsAntioxidantsAscorbic AcidBlood-Testis BarrierCadmiumCadmium ChlorideCatalaseMaleMalondialdehydeMAP Kinase Signaling SystemOxidative Stressp38 Mitogen-Activated Protein KinasesProtective AgentsRats, Sprague-DawleySuperoxide DismutaseTestisAntioxidantsAscorbic AcidCadmiumCadmium ChlorideCatalaseMalondialdehydep38 Mitogen-Activated Protein KinasesProtective AgentsSuperoxide DismutaseAscorbic acidBlood-testis barrierCadmiumOxidative stressp38 MAPK

Identifiers

PMID29790047
OpenAlexW2803981780

What OpenQuestion holds

Textmetadata
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.