Molecular mechanisms of lead neurotoxicity

Miriam Beatriz Virgolini, Michael Aschner

Research output: Chapter in Book/Report/Conference proceedingChapter

13 Scopus citations


Lead (Pb2 +) is a non-essential metal with numerous industrial applications that have led to its ubiquity in the environment. Thus, not only occupational-exposed individuals’ health is compromised, but also that of the general population and in particular children. Notably, although the central nervous system is particularly susceptible to Pb2 +, other systems are affected as well. The present study focuses on molecular mechanisms that underlie the effects that arise from the presence of Pb2 + in situ in the brain, and the possible toxic effects that follows. As the brain barriers represent the first target of systemic Pb2 +, mechanisms of Pb2 + entry into the brain are discussed, followed by a detailed discussion on neurotoxic mechanisms, with special emphasis on theories of ion mimicry, mitochondrial dysfunction, redox imbalance, and neuroinflammation. Most importantly, the confluence and crosstalk between these events is combined into a cogent mechanism of toxicity, by intertwining recent and old evidences from humans, in vitro cell culture and experimental animals. Finally, pharmacological interventions, including chelators, antioxidants substances, anti-inflammatory drugs, or their combination are reviewed as integrated approaches to ameliorate Pb2 + harmful effects in both developing or adult organisms.

Original languageEnglish (US)
Title of host publicationNeurotoxicity of Metals
Subtitle of host publicationOld Issues and New Developments
EditorsMichael Aschner, Lucio G. Costa, Lucio G. Costa
PublisherElsevier Inc.
Number of pages55
ISBN (Print)9780128237755
StatePublished - Jan 2021

Publication series

NameAdvances in Neurotoxicology
ISSN (Electronic)2468-7480


  • Anti-inflammatory drugs
  • Antioxidants
  • Chelators
  • Ion mimicry
  • Lead
  • Metals
  • Mitochondrial dys-function
  • Neuroinflammation
  • Neurotoxicity
  • Redox imbalance

ASJC Scopus subject areas

  • Neuroscience (miscellaneous)
  • Health, Toxicology and Mutagenesis


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