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Updated: Jan 26, 2026

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Cell Labeling and Targeting with Superparamagnetic Iron Oxide Nanoparticles
Published on: October 19, 2015
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Iron Oxide Nanoparticles Affects Behaviour and Monoamine Levels in Mice
Vijayprakash Manickam1, Vasanth Dhakshinamoorthy1, Ekambaram Perumal2
1Molecular Toxicology Laboratory, Department of Biotechnology, Bharathiar University, Coimbatore, Tamil Nadu, 641 046, India.
Neurochemical Research
|April 4, 2019
Summary
Iron oxide nanoparticles (Fe2O3 NPs) impair motor coordination and memory in mice. These effects are linked to neuronal damage, disrupted ion balance, and altered neurotransmitter levels.
Area of Science:
- Nanomedicine
- Neuroscience
- Toxicology
Background:
- Iron oxide nanoparticles (Fe2O3 NPs) possess unique magnetic properties valuable in biomedical applications.
- While Fe2O3 NP neurotoxicity is known, the specific factors influencing neurobehavioral changes remain unclear.
Purpose of the Study:
- To investigate the neurobehavioral effects of oral Fe2O3 NP exposure in mice.
- To elucidate the underlying mechanisms of Fe2O3 NP-induced neurotoxicity.
Main Methods:
- Mice were administered Fe2O3 NPs (25 and 50 mg/kg) daily for 30 days via oral intubation.
- Neurobehavioral tests, brain tissue analysis (mitochondria, ATPase activity, ion homeostasis, myelin, protein expression), and neurotransmitter level assessments were performed.
Main Results:
- Fe2O3 NP exposure significantly impaired motor coordination and memory.
- Mitochondrial damage, reduced energy levels, and decreased ATPase activity were observed in brain regions.
- Disturbed ion homeostasis, axonal demyelination, altered intracellular calcium, and changes in dopamine, norepinephrine, and epinephrine levels were noted.
- Increased glial fibrillary acidic protein (GFAP) confirmed neuronal damage.
Conclusions:
- Oral exposure to Fe2O3 NPs induces significant neurobehavioral deficits in mice.
- Mechanisms include mitochondrial dysfunction, impaired ion homeostasis, demyelination, altered neurotransmitter systems, and neuronal damage.
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