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Updated: Apr 3, 2026
Functional Neuroimaging Using Ultrasonic Blood-brain Barrier Disruption and Manganese-enhanced MRI
Published on: July 12, 2012
Changes in Brain Metallome/Metabolome Pattern due to a Single i.v. Injection of Manganese in Rats
Katharina Neth1, Marianna Lucio1, Alesia Walker1
1Research Unit Analytical BioGeoChemistry, Helmholtz Zentrum München-German Research Center for Environment and Health (GmbH), Ingolstädter Landstrasse 1, D-85764, Neuherberg, Germany.
Abstract:
Exposure to high concentrations of Manganese (Mn) is known to potentially induce an accumulation in the brain, leading to a Parkinson related disease, called manganism. Versatile mechanisms of Mn-induced brain injury are discussed, with inactivation of mitochondrial defense against oxidative stress being a major one. So far, studies indicate that the main Mn-species entering the brain are low molecular mass (LMM) compounds such as Mn-citrate. Applying a single low dose MnCl2 injection in rats, we observed alterations in Mn-species pattern within the brain by analysis of aqueous brain extracts by size-exclusion chromatography--inductively coupled plasma mass spectrometry (SEC-ICP-MS). Additionally, electrospray ionization--ion cyclotron resonance-Fourier transform-mass spectrometry (ESI-ICR/FT-MS) measurement of methanolic brain extracts revealed a comprehensive analysis of changes in brain metabolisms after the single MnCl2 injection. Major alterations were observed for amino acid, fatty acid, glutathione, glucose and purine/pyrimidine metabolism. The power of this metabolomic approach is the broad and detailed overview of affected brain metabolisms. We also correlated results from the metallomic investigations (Mn concentrations and Mn-species in brain) with the findings from metabolomics. This strategy might help to unravel the role of different Mn-species during Mn-induced alterations in brain metabolism.
Insights
Manganese (Mn) exposure can cause Parkinson-like symptoms. This study reveals how Mn alters brain metabolism and species, offering insights into manganism mechanisms.
Area of Science:
- Neuroscience
- Toxicology
- Metabolomics
Background:
- High manganese (Mn) exposure can lead to manganism, a Parkinson-related neurological disorder.
- Mitochondrial dysfunction is a key mechanism in Mn-induced brain injury.
- Low molecular mass (LMM) Mn compounds, like Mn-citrate, are thought to be the primary species entering the brain.
Purpose of the Study:
- To investigate alterations in brain manganese (Mn) species and metabolism following a single low dose of MnCl2 in rats.
- To correlate metallomic findings (Mn concentration and species) with metabolomic changes.
- To elucidate the role of specific Mn species in Mn-induced brain metabolism alterations.
Main Methods:
- Rats received a single low dose of Manganese Chloride (MnCl2).
- Aqueous brain extracts were analyzed using size-exclusion chromatography coupled with inductively coupled plasma mass spectrometry (SEC-ICP-MS) to determine Mn species.
- Methanolic brain extracts were analyzed using electrospray ionization-ion cyclotron resonance-Fourier transform mass spectrometry (ESI-ICR/FT-MS) for comprehensive metabolomic profiling.
Main Results:
- A single low dose of MnCl2 altered the pattern of Mn species in rat brain extracts.
- Significant changes were observed in amino acid, fatty acid, glutathione, glucose, and purine/pyrimidine metabolism.
- Metallomic and metabolomic data were correlated to understand Mn-species impact on brain metabolism.
Conclusions:
- This study provides a broad overview of Mn-induced metabolic disturbances in the brain.
- The findings highlight the potential role of specific Mn species in neurotoxicity.
- The combined metallomic and metabolomic approach aids in understanding the mechanisms of manganism.
