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Diverse Serum Manganese Species Affect Brain Metabolites Depending on Exposure Conditions
Katharina Neth, Marianna Lucio, Alesia Walker
1§Technische Universität München, Chair of Analytical Food Chemistry, Alte Akademie 10, D-85354 Freising, Germany.
Abstract:
Occupational and environmental exposure to increased concentrations of manganese (Mn) can lead to an accumulation of this element in the brain. The consequence is an irreversible damage of dopaminergic neurons leading to a disease called manganism with a clinical presentation similar to the one observed in Parkinson's disease. Human as well as animal studies indicate that Mn is mainly bound to low molecular mass (LMM) compounds such as Mn-citrate when crossing neural barriers. The shift toward LMM compounds might already take place in serum due to elevated Mn concentrations in the body. In this study, we investigated Mn-species pattern in serum in two different animal models by size exclusion chromatography-inductively coupled plasma mass spectrometry (SEC-ICP-MS). A subchronic feeding of rats with elevated levels of Mn led to an increase in LMM compounds, mainly Mn-citrate and Mn bound to amino acids. In addition, a single i.v. injection of Mn showed an increase in Mn-transferrin and Mn bound to amino acids 1 h after injection, while species values were more or less rebalanced 4 days after the injection. Results from Mn-speciation were correlated to the brain metabolome determined by means of electrospray ionization ion cyclotron resonance Fourier transform mass spectrometry (ESI-ICR/FT-MS). The powerful combination of Mn-speciation in serum with metabolomics of the brain underlined the need for Mn-speciation in exposure scenarios instead of the determination of whole Mn concentrations in blood. The progress of Mn-induced neuronal injury might therefore be assessed on the basis of known serum Mn-species.
Insights
Manganese (Mn) exposure can damage brain neurons, causing manganism similar to Parkinson's disease. Measuring specific manganese compounds in serum, not just total levels, can help assess this neurotoxicity.
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- Occupational and environmental manganese (Mn) exposure leads to brain accumulation and dopaminergic neuron damage.
- This neurotoxicity causes manganism, a condition clinically resembling Parkinson's disease.
- Manganese crosses neural barriers primarily bound to low molecular mass (LMM) compounds like Mn-citrate.
Purpose of the Study:
- To investigate manganese species patterns in serum using two animal models.
- To correlate serum manganese speciation with brain metabolome changes.
- To evaluate the utility of serum Mn-speciation for assessing neurotoxicity.
Main Methods:
- Size exclusion chromatography-inductively coupled plasma mass spectrometry (SEC-ICP-MS) for serum Mn-speciation.
- Subchronic Mn feeding in rats and single intravenous Mn injection in animal models.
- Brain metabolomics using electrospray ionization ion cyclotron resonance Fourier transform mass spectrometry (ESI-ICR/FT-MS).
Main Results:
- Subchronic Mn feeding increased LMM compounds (Mn-citrate, Mn-amino acids) in rat serum.
- Acute Mn injection transiently altered serum species (increased Mn-transferrin, Mn-amino acids) before rebalancing.
- Serum Mn-speciation patterns correlated with brain metabolomic profiles.
Conclusions:
- Serum Mn-speciation provides a more accurate assessment of Mn exposure and neurotoxicity than total Mn concentration.
- Monitoring specific serum Mn-species can potentially track the progression of Mn-induced neuronal injury.
- This approach aids in understanding Mn transport and its neurological impact in exposure scenarios.
