open access

Vol 46, No 6 (2012)
ARTYKUŁ POGLĄDOWY
Submitted: 2012-02-04
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Neurotoxicity of lead. Hypothetical molecular mechanisms of synaptic function disorders

Irena Baranowska-Bosiacka1, Izabela Gutowska2, Marta Rybicka1, Przemysław Nowacki3, Dariusz Chlubek1
DOI: 10.5114/ninp.2012.31607
·
Neurol Neurochir Pol 2012;46(6):569-578.
Affiliations
  1. Katedra Biochemii i Chemii Medycznej, Pomorski Uniwersytet Medyczny w Szczecinie
  2. Zakład Biochemii i Żywienia Człowieka, Pomorski Uniwersytet Medyczny w Szczecinie
  3. Katedra i Klinika Neurologii w Zabrzu, Śląski Uniwersytet Medyczny w Katowicach

open access

Vol 46, No 6 (2012)
ARTYKUŁ POGLĄDOWY
Submitted: 2012-02-04

Abstract

Lead (Pb) toxicity is still a major health problem associated with both environmental and occupational exposure. Special attention is given to the neurotoxic effect of lead. Along with the newly emerging data, the Pb concentration in the body that can be considered safe is declining. Numerous studies on the neurotoxicity of Pb have shown multiple cellular ‘molecular targets’ of this metal at the biochemical and molecular levels, and differences in sensitivity to its toxic action among various neural cells. One possible target of the neurotoxic effect of Pb (at the synapse level) is N-methyl-D-aspartic acid (NMDA) receptors. This review presents the hypothetical molecular mechanism by which Pb disrupts synapse formation and plasticity in developing hippocampal neurons and the role of the NMDA receptor-dependent signaling pathway and brain-derived neurotrophic factor (BDNF) as a mechanism of Pb neurotoxicity at the synapse level.

Abstract

Lead (Pb) toxicity is still a major health problem associated with both environmental and occupational exposure. Special attention is given to the neurotoxic effect of lead. Along with the newly emerging data, the Pb concentration in the body that can be considered safe is declining. Numerous studies on the neurotoxicity of Pb have shown multiple cellular ‘molecular targets’ of this metal at the biochemical and molecular levels, and differences in sensitivity to its toxic action among various neural cells. One possible target of the neurotoxic effect of Pb (at the synapse level) is N-methyl-D-aspartic acid (NMDA) receptors. This review presents the hypothetical molecular mechanism by which Pb disrupts synapse formation and plasticity in developing hippocampal neurons and the role of the NMDA receptor-dependent signaling pathway and brain-derived neurotrophic factor (BDNF) as a mechanism of Pb neurotoxicity at the synapse level.

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Keywords

lead (Pb), neurotoxicity, NMDA receptor, BDNF, brain, hippocampus

About this article
Title

Neurotoxicity of lead. Hypothetical molecular mechanisms of synaptic function disorders

Journal

Neurologia i Neurochirurgia Polska

Issue

Vol 46, No 6 (2012)

Pages

569-578

Page views

751

Article views/downloads

917

DOI

10.5114/ninp.2012.31607

Bibliographic record

Neurol Neurochir Pol 2012;46(6):569-578.

Keywords

lead (Pb)
neurotoxicity
NMDA receptor
BDNF
brain
hippocampus

Authors

Irena Baranowska-Bosiacka
Izabela Gutowska
Marta Rybicka
Przemysław Nowacki
Dariusz Chlubek

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