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HERO ID
2950383
Reference Type
Journal Article
Subtype
Review
Title
The Physiopathologic Significance of Manganese in Brain: Its Relation to Schizophrenia and Neurodegenerative Disorders
Author(s)
Donaldson, J
Year
1987
Is Peer Reviewed?
1
Journal
NeuroToxicology
ISSN:
0161-813X
EISSN:
1872-9711
Report Number
NIOSH/00172068
Volume
8
Issue
3
Page Numbers
451-462
Language
English
PMID
3309736
Web of Science Id
WOS:A1987J585700013
URL
https://www.ncbi.nlm.nih.gov/pubmed/3309736
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Abstract
The physiopathology of elevated brain manganese (7439965) (Mn) was reviewed with the purpose of elucidating mechanisms of Mn neurotoxicity. Animal models of Mn pathology, case studies of Locura-manganica or manganese madness, the Groote Eylandt syndrome, chronic manganism, and manganese psychosis were discussed. Common observations included melanin loss, degeneration of the striatum or its components, and alterations in central dopaminergic receptors implying dopamine oxidation as a mechanism of Mn pathology. Hypotheses for Mn pathology reviewed included Mn induced enhancement of dopamine autooxidation, Mn catalyzed production of toxic catecholamines, Mn self oxidation and dismutation with resulting oxidative destruction of dopamine, and catecholamine oxidation by trivalent Mn. The role of zinc in protecting against Mn induced dopamine oxidation was attributed to the affinity of zinc ions for hydroxyl moieties and to the involvement of zinc in maintaining redox balance and membrane stability. The author suggests that tissue susceptibility to Mn toxic effects in the brain are related to the redox bioenergetic status of the various tissues and that other tissues with elevated levels of oxidative enzymes (oxidases, peroxides) such as testes, pancreatic-B cells, and macrophages would show similar sensitivity to Mn insult.
Keywords
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Animals; Blood Glucose/metabolism; Brain/physiopathology; Brain Chemistry; Disease Models, Animal; Dopamine/metabolism; Manganese Poisoning; Nerve Degeneration/drug effects; Oxidation-Reduction; Psychomotor Disorders/chemically induced; Psychoses, Substance-Induced/metabolism; Pyridines/pharmacology; Schizophrenia/chemically induced; Zinc/physiology
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