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Updated: Feb 27, 2026
Functional Neuroimaging Using Ultrasonic Blood-brain Barrier Disruption and Manganese-enhanced MRI
Published on: July 12, 2012
Disrupted Tryptophan Metabolism Mediates Manganese-Induced Neurogenesis and Neuroinflammatory Impairments: Rescue by
Xueting Wang1,2, Teng Ma1,2, Weifeng He1,2
1Department of Occupational Health and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China.
Abstract:
Manganese (Mn) is a common environmental pollutant, and excessive exposure can lead to motor dysfunction resembling Parkinson's disease. Increasing evidence suggests that Mn impairs endogenous neurogenesis and hinders neural repair. This study aims to investigate the effects of both acute and long-term Mn exposure on neurogenesis and to elucidate the underlying mechanisms. By establishing acute (7 and 14 days) and long-term (2 and 4 months) Mn exposure mouse models, we assessed neurogenesis under different exposure conditions. The mRNA sequencing, untargeted metabolomics, and metagenomics were employed to uncover the molecular pathways involved in Mn-induced neurogenesis impairment. The results revealed that early stage Mn exposure, including acute and 2 months exposure, transiently promoted neurogenesis. However, prolonged Mn accumulation in the brain led to suppressed neurogenesis, accompanied by neuroinflammation and oxidative stress, which contributed to a vicious cycle of neural damage. Multiomics analyses identified dysregulation of the tryptophan metabolic pathway as a key mechanism, with a marked reduction in melatonin levels following Mn exposure. Notably, exogenous melatonin supplementation effectively rescued Mn-induced impairments in neurogenesis, neuronal integrity, and neuroinflammation. These findings provide new insights into Mn neurotoxicity and highlight melatonin as a potential therapeutic agent for Mn-related neural damage.
Insights
Manganese (Mn) exposure initially boosts neurogenesis but prolonged exposure impairs it, causing neural damage. Melatonin supplementation effectively reversed these harmful effects, offering a potential treatment for manganese neurotoxicity.
Area of Science:
- Neuroscience
- Environmental Health
- Toxicology
Background:
- Manganese (Mn) is an environmental pollutant linked to Parkinson's-like motor dysfunction.
- Mn exposure is known to impair neurogenesis and neural repair processes.
- Understanding Mn's impact on the brain is crucial for developing effective interventions.
Purpose of the Study:
- To investigate the dual effects of acute and long-term manganese exposure on neurogenesis.
- To elucidate the molecular mechanisms underlying manganese-induced neurogenesis impairment.
- To evaluate melatonin as a potential therapeutic agent against manganese neurotoxicity.
Main Methods:
- Established acute (7, 14 days) and long-term (2, 4 months) manganese exposure mouse models.
- Utilized mRNA sequencing, untargeted metabolomics, and metagenomics for multiomics analysis.
- Assessed neurogenesis, neuroinflammation, oxidative stress, and neuronal integrity.
Main Results:
- Early Mn exposure (acute, 2 months) transiently promoted neurogenesis.
- Prolonged Mn exposure suppressed neurogenesis, inducing neuroinflammation and oxidative stress.
- Dysregulation of tryptophan metabolism and reduced melatonin were key findings; melatonin supplementation rescued Mn-induced damage.
Conclusions:
- Manganese neurotoxicity involves a biphasic effect on neurogenesis, with prolonged exposure leading to detrimental outcomes.
- Disruption of the tryptophan-melatonin pathway is a critical mechanism in Mn-induced neurotoxicity.
- Melatonin shows significant therapeutic potential for mitigating manganese-related neural damage.
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