To examine how disturbances in metal homeostasis reshape metabolic pathways in Caenorhabditis elegans.
Key Findings:
Zinc is a central regulator of metal balance, with iron and manganese exposure reducing total zinc levels.
Zinc treatment alters the distribution of iron and manganese species within cells.
Chronic iron exposure leads to significant shifts in metabolites linked to central carbon metabolism, indicating impaired energy metabolism.
Manganese exposure causes subtler metabolic changes, while zinc treatment results in modest disruptions.
Interpretation:
Neurons may be particularly sensitive to metabolic strain from disrupted metal homeostasis, potentially linking metal imbalance to neurodegenerative processes.
Limitations:
Findings are limited to the model organism C. elegans.
Further research is needed to extend these findings to other systems.
Conclusion:
Combining metal speciation analysis with untargeted metabolomics offers a structured approach to studying metal–metabolism interactions, with implications for understanding aging and neurodegeneration.
