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Manganese catalyzed auto-oxidation of dopamine to 6-hydroxydopamine in vitro
1Biomedical Science Department, General Motors Research Laboratories, Warren, MI 48090-9058.
Abstract:
Manganese (Mn) is an essential trace element which, upon excessive exposure, produces a neurological syndrome similar to chronic Parkinson's disease in animals and humans. Previous work demonstrated that Mn was more potent than other transition metals in stimulating dopamine (DA) auto-oxidation. In these experiments, DA was incubated under physiological conditions in the presence and absence of Mn for up to 60 min. 6-Hydroxydopamine (6-OHDA) was produced in the presence of Mn, while the incubation mixture without Mn showed no DA oxidation. 6-Hydroxydopamine is a neurotoxicant which exerts its effects by destroying DA nerve terminals in the CNS. Therefore, this work suggests that the Mn catalyzed increase in DA auto-oxidation could be linked mechanistically to the appearance of Mn-induced neurotoxic effects.
Insights
Excess manganese exposure can cause Parkinson
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- Manganese (Mn) is essential but toxic in excess.
- Excess Mn exposure causes neurological issues similar to Parkinson's disease.
- Mn is potent in stimulating dopamine (DA) auto-oxidation.
Purpose of the Study:
- To investigate the mechanism linking manganese exposure to neurotoxicity.
- To determine if Mn catalyzes dopamine auto-oxidation.
Main Methods:
- Incubating dopamine (DA) under physiological conditions.
- Comparing DA oxidation in the presence and absence of Mn.
- Measuring the production of 6-hydroxydopamine (6-OHDA).
Main Results:
- Manganese (Mn) significantly increased dopamine (DA) auto-oxidation.
- 6-Hydroxydopamine (6-OHDA), a neurotoxicant, was produced in the presence of Mn.
- No DA oxidation occurred without Mn.
Conclusions:
- Mn catalyzes DA auto-oxidation.
- This Mn-induced DA oxidation may mechanistically explain Mn neurotoxicity.
- This links Mn exposure to Parkinson's-like symptoms.