ElMosbah et al. 2024 - Aluminum chloride rat neurotoxicity and rivastigmine chitosan nanoparticles

ElMosbah and colleagues used oral aluminum chloride to induce Alzheimer’s-like pathology in rats, then compared oral versus intranasal rivastigmine-loaded chitosan nanoparticles. This is in-scope lane a4 toxicology evidence for aluminum neurotoxicity and treatment response. It is not consumer-product occurrence evidence and does not report aluminum concentrations in food, water, or tissue.

Key numbers

The model used 30 adult male albino rats weighing 200-250 g. Rats acclimatized for 7 days before the experiment.

The experimental design section reports these exposure and treatment values:

The methods report chitosan solutions prepared at 0.5%, 0.7%, 1%, 1.2%, and 1.4% w/v, and sodium tripolyphosphate solutions prepared at 0.6%, 0.8%, 1%, 1.2%, and 1.4% w/v. Tween 80 was added at a constant ratio of 0.2 mL.

Table 1 gives real-time PCR primer product sizes:

The results state that viable neuron percentage was significantly reduced in the AlCl3 group compared with other groups, and that AlCl3 + nasal RS-CSNPs had significantly higher cell viability and less neuronal degeneration than AlCl3 + oral RS-CSNPs. The figure with neuron viability percentages is graphical; exact numeric percentages are not reported in extractable text.

The qPCR results state that Caspase-3 and NF-kB expression were significantly up-regulated in the AlCl3 group compared with treated and control groups, while Nrf-2 was significantly down-regulated in the AlCl3 group. The source reports that Caspase-3 transcript fold change was significantly lower in AlCl3 + nasal RS-CSNPs than in AlCl3 + oral RS-CSNPs, while NF-kB and Nrf-2 did not significantly differ between the two treated AlCl3 subgroups. The fold-change values are shown in bar charts and are not printed as exact text values.

Methods (brief)

The study was conducted in the Pathology Department, Faculty of Veterinary Medicine, Cairo University. Brain, nasal mucosa, stomach, intestine, and liver were fixed in 10% neutral buffered formalin, embedded in paraffin, sectioned at 3-4 um, and stained with H&E. Cresyl violet (Nissl) staining was used to quantify viable neurons in cerebral cortical regions. Phosphorylated tau expression was assessed by immunohistochemistry using a 1:100 phosphorylated tau antibody. Gene expression for Caspase-3, NF-kB, and Nrf-2 was measured by real-time PCR and normalized to beta-actin.

Implications

Certification: Do not use this source for any product threshold, occurrence pool, or aluminum concentration estimate. The aluminum exposure was an oral AlCl3 animal-model dose, not a measured food or consumer-product contaminant.

Courses: Useful downstream-effect example for explaining why aluminum toxicology is tracked separately from product occurrence. It also shows the firewall: treatment-response and biomarker endpoints belong on metal toxicology surfaces, not in product contamination tables.

App: Context only. The source can inform aluminum toxicology background but cannot score ingredients or products.

Wiki pages this source may touch

• aluminum
• aluminum-toxicology

Verification notes

Recovered from skip:no-occurrence-data under the 2026-06-10 inclusion-by-default rule. On reading, this paper is lane a4 toxicology evidence because it uses AlCl3 to induce an Alzheimer’s-like rat model and reports histopathology, tau immunohistochemistry, and gene-expression response.

Numbers were checked against the abstract, nanoparticle-preparation section, experimental-design section, Table 1, results text, and figure captions. No food, water, product, or tissue aluminum concentration is reported, and no exact figure-bar values are transcribed because they are not printed in the extracted text. Products and ingredients are intentionally empty.

Page history

The five most recent substantive edits to this page. The full version history lives in git; when DOI minting comes online (see schema docs), each entry below will also link to a version-pinned DataCite DOI.