Evidence map›Paper›PMID 32440822›Full record

ArticleJournal of molecular neuroscience : MN2020

Neurotoxic, Hepatotoxic and Nephrotoxic Effects of Tramadol Administration in Rats.

Haytham A Ali, Mohamed Afifi, Taghred M Saber, Arwa A Makki, A T Keshta, Mohammed Baeshen, Ammar Al-Farga

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Biochemical and Histopathological Alterations Induced by Tramadol.Medical journal of the Islamic Republic of Iran · 2025
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  7. Review
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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

7 authors at 2 institutions in 2 countries.

Haytham A AliCollege of Science, Department of Biochemistry, University of Jeddah, Jeddah, Saudi Arabia. hagad@uj.edu.sa.ORCID http://orcid.org/0000-0002-0233-5539
Mohamed AfifiCollege of Science, Department of Biochemistry, University of Jeddah, Jeddah, Saudi Arabia.
Taghred M SaberDepartment of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Zagazig University, Zagazig, 44519, Egypt.
Arwa A MakkiCollege of Science, Department of Biochemistry, University of Jeddah, Jeddah, Saudi Arabia.
A T KeshtaDepartment of Biochemistry, Faculty of Science, Zagazig University, Zagazig, 44519, Egypt.
Mohammed BaeshenCollege of Science, Department of Biology, University of Jeddah, Jeddah, Saudi Arabia.
Ammar Al-FargaCollege of Science, Department of Biochemistry, University of Jeddah, Jeddah, Saudi Arabia.
Zagazig University · EGUniversity of Jeddah · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The current study was performed to study the tramadol HCL toxic effects on the brain, liver, and kidney of adult male rats. Forty male adult albino rats were divided into 4 groups; the first one was considered as a control group, the others were orally administrated with 25, 50, and 100 b.wt. representing therapeutic, double therapeutic, and 4 times therapeutic doses, respectively, of tramadol HCL daily for 1 month. Serum and brain, hepatic, and renal tissues were collected for biochemical and molecular investigations. Tramadol HCL resulted in a significant increase in the brain serotonin, 8-hydroxy-2'-deoxyguanosine (8-OHdG), and malonyldialdehyde (MDA) levels with a significant decrease in the reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) activities. At the same line, hepatic and renal 8-OHdG and MDA levels showed a significant increase with a significant decrease in reduced glutathione (GSH), CAT, and SOD activities. In addition, hepatic and renal function parameters including serum alanine amino transferase (ALT), aspartate amino transferase (AST), urea, and creatinine were increased in a dose-dependent manner. At the molecular levels, hepatic cytochrome P5402E1 (CYP2E1), renal Kidney Injury Molecule-1 (KIM-1), and tissue inhibitor of metalloproteinase-1 (TIMP-1) showed also a significant increase in the expression levels. Histopathological evaluation of the brain confirmed the above biochemical results. In conclusion, tramadol HCL induced neurotoxic, hepatotoxic, and nephrotoxic effects in a manner relative to its concentration by affecting brain serotonin levels and hepatic and renal function, with the production of DNA damage and oxidative stress.

Indexed as

8-Hydroxy-2'-DeoxyguanosineAlanine TransaminaseAnalgesics, OpioidAnimalsBrainCatalaseCell Adhesion MoleculesCytochrome P-450 CYP2E1GlutathioneKidneyLiverMaleRatsSerotoninSuperoxide DismutaseTissue Inhibitor of Metalloproteinase-18-Hydroxy-2'-DeoxyguanosineAlanine TransaminaseAnalgesics, OpioidCatalaseCell Adhesion MoleculesCytochrome P-450 CYP2E1GlutathioneHavcr1 protein, ratSerotoninSuperoxide DismutaseTIMP1 protein, ratTissue Inhibitor of Metalloproteinase-1Tramadol8-OHdGCYP2E1KIM-1SerotoninTIMP-1Tramadol HCL

Identifiers

PMID32440822
OpenAlexW3026055040

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.