Evidence map›Paper›PMID 39937257›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2025

Polyethylene terephthalate nanoplastics-induced neurotoxicity in adult male Swiss albino mice with amelioration of betaine: a histopathological, neurochemical, and molecular investigation.

Nehal A Kamel, Dina W Bashir, Ebtihal M M El-Leithy, Adel F Tohamy, Maha M Rashad, Ghada E Ali, Abdel Aleem A El-Saba

Abstract read
In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Overall effects of microplastics on brain.Frontiers in toxicology · 2025
    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

7 authors.

Nehal A KamelDepartment of Cytology and Histology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt. nehalalsayed@cu.edu.eg.
Dina W BashirDepartment of Cytology and Histology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt.
Ebtihal M M El-LeithyDepartment of Cytology and Histology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt.
Adel F TohamyDepartment of Toxicology and Forensic Medicine, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt.
Maha M RashadDepartment of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt.
Ghada E AliDepartment of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt.
Abdel Aleem A El-SabaDepartment of Cytology and Histology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Medicines, food packaging, personal care products, and cosmetics extensively use polyethylene terephthalate nanoplastics (PET-NaPs). However, they also have harmful impacts on several organs. Betaine demonstrates potent antioxidant and anti-inflammatory characteristics. Our goal was to investigate the detrimental impact of PET-NaPs on the mouse brain and evaluate the neuroprotective properties of betaine. We allocated 40 completely mature male Swiss albino mice into four distinct groups: control group, betaine group, PET-NaPs group, and betaine-co-treated group. Following a 30-day duration, euthanasia was performed on the mice, and analyzed tissue samples were obtained from the cerebrum, cerebellum, and hippocampus. PET-NaPs resulted in an elevated level of malondialdehyde and upregulated cyclooxygenase-2 and interleukin-1 beta (IL-1β) expression while significantly reducing the levels of glutathione and downregulating acetylcholinesterase. The PET-NPs also caused significant changes in the histopathology of the brain tissue, and there was a demonstrable rise in the immunostaining of IL-1β and glial fibrillary acidic proteins. Consequently, betaine effectively alleviated the negative consequences of PET-NaPs. Therefore, betaine possesses the capacity to mitigate the neurotoxic consequences induced by PET-NaPs.

Indexed as

AntioxidantsBetaineBrainMicroplasticsNeuroprotective AgentsNeurotoxicity SyndromesPolyethylene TerephthalatesAcetylcholinesteraseAnimalsCyclooxygenase 2Glial Fibrillary Acidic ProteinGlutathioneInterleukin-1betaMaleMalondialdehydeMiceAcetylcholinesteraseAntioxidantsBetaineCyclooxygenase 2Glial Fibrillary Acidic ProteinGlutathioneIL1B protein, mouseInterleukin-1betaMalondialdehydeMicroplasticsNeuroprotective AgentsPolyethylene TerephthalatesPtgs2 protein, mouseBetaineNeurochemical markersNeurotoxicityPolyethylene terephthalate nanoplastics

Identifiers

PMID39937257
PMCPMC12263730

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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.