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Yuan et al. 2012 — Aluminum Overload and Oxidative Stress in Neonatal Rat Brains

This 2012 Taiwanese animal study demonstrated dose-dependent aluminum accumulation and oxidative stress (measured as TBARS/lipid peroxidation) in multiple brain regions of neonatal rats. This is an animal toxicology study; it provides mechanistic support for Al neurotoxicity in early development but does not provide food or formula concentration data.

Key numbers

Brain Al concentrations after intraperitoneal AlCl3 (ng/g wet weight):

RegionControlHigh Al (35 mg/kg/day)p
Hippocampus294.9 ± 180.8751.0 ± 225.8<0.05
Diencephalon20.4 ± 9.679.6 ± 20.7<0.05
Cerebellum83.1 ± 15.2144.8 ± 36.2<0.05
Whole brain219.5 ± 43.1

TBARS (lipid peroxidation) increased significantly in hippocampus, diencephalon, cerebellum, and brain stem in the high-Al group.

Methods

Intraperitoneal AlCl3 injection PND3–17. AAS or ICP (not specified). Wet weight. Animal study; intraperitoneal route does not replicate oral dietary exposure. Dose of 35 mg Al/kg/day far exceeds human dietary exposure from formula (typically <7 mg/L Al in formula × consumption). Results support the mechanistic plausibility of Al neurotoxicity but cannot directly inform food safety thresholds.

Implications

Health: Provides mechanistic evidence for Al-induced oxidative stress and neural regional vulnerability in early development; supports precautionary concern about high Al in infant formula.

Certification: Cannot be used directly for HMT&C Al thresholds (animal, intraperitoneal route). Relevant to the biological plausibility section of Al toxicology pages.

Wiki pages updated on ingest

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.

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b0f3d382026-06-12batch | corpus rescreen b04 old terminal skips