Evidence map›Paper›PMID 40892347›Full record

ArticleMetabolic brain disease2025

Zinc oxide nanoparticles exposure disrupts brain redox-inflammatory-epigenetic axis and impairs PI3K/Akt survival pathway in male offspring.

Norah Saeed Al-Zahrani, Hind Zafrah, Alshehri Hanan Hassan, Eman Mohamad El Nashar, Hanan M A El Henafy

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Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–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

5 citing papers in PubMed.

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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

5 authors.

Norah Saeed Al-ZahraniDepartment of Clinical Biochemistry, College of Medicine, King Khalid University, Abha, 62529, Saudi Arabia.
Hind ZafrahDepartment of Physiology, Faculty of Medicine, King Khalid University, Abha, 62529, Saudi Arabia.ORCID 0009-0002-6987-6222
Alshehri Hanan HassanEndocrinology and Diabetes Section, Internal Medicine Department, College of Medicine, King Khalid University, Abha, 62529, Saudi Arabia.ORCID 0000-0001-8931-3545
Eman Mohamad El NasharDepartment of Anatomy, College of Medicine, King Khalid University, Abha, 62529, Saudi Arabia. enshar@kku.edu.sa.ORCID 0000-0002-2883-6761
Hanan M A El HenafyTechnology of Medical Laboratory Department, Faculty of Technology of Applied Health Sciences, October 6 University, Giza, 3230911, Egypt. Hanan.Mohammed.AMS@o6u.edu.eg.ORCID 0000-0003-0838-016X

Funding

Deanship of Research and Graduate Studies at King Khalid University RGP2/536/46
6 · The paper itself

Abstract

Widespread use of Zinc Oxide Nanoparticles (ZnO NPs) raises concerns about potential health risks, particularly following maternal exposure during critical developmental windows. The impact of exposure on offspring brain development remains unclear. The work aims to investigate the neurodevelopmental consequences of maternal ZnO NP exposure during gestation, lactation, or both periods in male rat offspring. Pregnant rats were administered ZnO NPs (< 100 nm) or vehicle. Offspring developmental parameters and brain tissues were analyzed at postnatal day 60. Assessments included oxidative stress markers (8-OHdG, MDA, NO), antioxidant (GSH, GST, GPX, SOD, CAT), cholinergic function (AChE), epigenetic markers (DNA methylation, BDNF promoter methylation, miR-34a, miR-29b), neurodegeneration-associated proteins (Aβ1-42, Tau), survival/inflammatory signaling pathways (p-Akt, PI3K mRNA, ERK, Bcl-2, COX2, IL-1β, TNF-α, IL-2, TGF-β), apoptosis (Caspase-3), BDNF mRNA, and brain histology. Maternal ZnO NP exposure significantly reduced offspring brain weight, body weight, and survival index, particularly following combined gestational and lactational exposure. Exposed offspring brains exhibited increased oxidative stress, depleted antioxidant defenses, impaired AChE activity, global DNA hypomethylation with targeted BDNF promoter hypermethylation (correlating with reduced BDNF mRNA), increased Aβ1-42 and Tau accumulation, suppressed PI3K/p-Akt and ERK survival signaling, elevated pro-inflammatory markers (IL-1β, TNF-α, IL-2, COX2, TGF-β), increased apoptosis (Caspase-3) alongside decreased Bcl-2, and dysregulated miRNA expression (increased miR-34a, decreased miR-29b). Histology confirmed duration-dependent neuronal damage. Maternal ZnO NP exposure induces persistent offspring neurotoxicity via oxidative stress, neuroinflammation, apoptosis, and epigenetic dysregulation. This highlights developmental brain vulnerability and the importance of assessing maternal nanoparticle exposure.

Indexed as

BrainEpigenesis, GeneticMetal NanoparticlesNanoparticlesPhosphatidylinositol 3-KinasesPrenatal Exposure Delayed EffectsProto-Oncogene Proteins c-aktZinc OxideAnimalsFemaleInflammationMaleOxidation-ReductionOxidative StressPregnancyRatsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktZinc OxideGreen toxicologyNeurodevelopmental toxicityNeuroinflammationOxidative stressZinc oxide nanoparticles (ZnO NPs)

Identifiers

PMID40892347

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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.