Manganese neurotoxicity: Cellular effects and blood-brain barrier transport

Michael Aschner, Judy L. Aschner

Research output: Contribution to journalArticle

229 Scopus citations

Abstract

The observations by Couper in 1837 are acknowledged as the earliest description of the toxic syndrome associated with chronic manganese (Mn) exposure. Since that time, many of the neurotoxic aspects of manganism have been described, yet, the primary basis for its neurotoxicity remains unknown. Recent evidence corroborates the original hypothesis by Maynard and Cotzias (82) which invokes the mitochondrion as the target organelle for Mn cytotoxicity which is primarily expressed as a perturbation in Ca2+ homeostasis. Despite recognition that excessive Mn exposure culminates in Mn accumulation in the CNS and a clinical picture dominated by neurological disturbances, the role of the blood-brain barrier in the CNS uptake of Mn has received little attention. Accordingly, the first part of this review summarizes the current understanding of the interaction of Mn with biologically active sites in the induction of Mn cytotoxicity. The second part of this review summarizes what is known about Mn transport across the blood-brain barrier, a major regulator of the CNS milieu, with the contention that the rate and extent of Mn transport across the blood-brain barrier modulates its neurotoxicity.

Original languageEnglish (US)
Pages (from-to)333-340
Number of pages8
JournalNeuroscience and Biobehavioral Reviews
Volume15
Issue number3
DOIs
StatePublished - Jan 1 1991

Keywords

  • Blood-brain barrier
  • Manganese
  • Mitochondria
  • Neurotoxicity
  • Transferrin
  • Transport

ASJC Scopus subject areas

  • Neuropsychology and Physiological Psychology
  • Cognitive Neuroscience
  • Behavioral Neuroscience

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