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Methylmercury Neurotoxicity: Exploring Potential Novel Targets.
J L Aschner1, M Aschner1,2
1Department of Pediatrics and the Kennedy Center for Research on Human Development.
The Open Toxicology Journal
|June 11, 2019
Summary
Methylmercury (MeHg) may disrupt central nervous system (CNS) function by interfering with chaperone proteins that regulate key cellular pathways. This offers a unifying mechanism for MeHg
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- Central nervous system (CNS) methylmercury (MeHg) toxicity mechanisms remain unclear.
- Nitric oxide synthase (NOS)-cyclic GMP and cyclooxygenase (COX)-prostaglandin (PG) pathways are crucial for CNS function.
- Chaperone proteins are essential for regulating these pathways via post-translational modifications.
Purpose of the Study:
- To explore the unexplored role of MeHg in altering chaperone-client protein interactions.
- To propose a unifying upstream mechanism for diverse MeHg effects.
- To investigate MeHg neurotoxicity in astrocytes as a model system.
Main Methods:
- Review of existing literature on MeHg effects, CNS signaling pathways, and chaperone proteins.
- Focus on the interaction of mercurials with sulfhydryl (-SH) groups.
- Examination of the role of molecular chaperones like heat shock protein 90 (Hsp90) in protein redox regulation.
Main Results:
- MeHg's affinity for sulfhydryl groups suggests interference with thiol-dependent protein functions.
- Chaperone proteins are critical for maintaining redox status and protein function.
- MeHg may disrupt chaperone-client protein interactions, impacting cellular homeostasis.
Conclusions:
- Interference with chaperone-client protein interactions presents a novel, unifying mechanism for MeHg neurotoxicity.
- Astrocytes are a relevant model for studying MeHg's impact on cellular homeostasis.
- This mechanism potentially explains MeHg-induced ROS generation, mitochondrial dysfunction, and other toxic effects.
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