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ToxSci Advance Access originally published online on October 17, 2006
Toxicological Sciences 2007 95(1):156-162; doi:10.1093/toxsci/kfl134
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© The Author 2006. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Inflammation-Like Glial Response in Lead-Exposed Immature Rat Brain

Lidia Struzynska1, Beata Dabrowska-Bouta, Katarzyna Koza and Grzegorz Sulkowski

Department of Neurochemistry, Medical Research Centre, Laboratory of Pathoneurochemistry, Polish Academy of Sciences, 02-106 Warsaw, Poland

1 To whom correspondence should be addressed at Department of Neurochemistry, Medical Research Centre, Laboratory of Pathoneurochemistry, Polish Academy of Sciences, 5 Pawinskiego str., 02-106 Warsaw, Poland. Fax: +48 22-668-54-23. E-mail: lidkas{at}cmdik.pan.pl.

Received July 21, 2006; accepted September 29, 2006


  Abstract

Numerous studies on lead (Pb) neurotoxicity have indicated this metal to be a dangerous toxin, particularly during developmental stages of higher organisms. Astrocytes are responsible for sequestration of this metal in brain tissue. Activation of astroglia may often lead to loss of the buffering function and contribute to pathological processes. This phenomenon is accompanied by death of neuronal cells and may be connected with inflammatory events arising from the production of a wide range of cytokines and chemokines. The effects of prolonged exposure to Pb upon glial activation are examined in immature rats to investigate this potential proinflammatory effect. When analyzed at the protein level, glial activation is observed after Pb exposure, as reflected by the increased level of glial fibrillary acidic protein and S-100ß proteins in all parts of the brain examined. These changes are associated with elevation of proinflammatory cytokines. Production of interleukin (IL)-1ß and tumor necrosis factor-{alpha} is observed in hippocampus, and production of IL-6 is seen in forebrain. The expression of fractalkine is observed in both hippocampus and forebrain but inconsiderably in the cerebellum. In parallel with cytokine expression, signs of synaptic damage in hippocampus are seen after Pb exposure, as indicated by decreased levels of the axonal markers synapsin I and synaptophysin. Obtained results indicate chronic glial activation with coexisting inflammatory and neurodegenerative features as a new mechanism of Pb neurotoxicity in immature rat brain.

Key Words: Pb neurotoxicity; cytokines; neuroinflammation; S-100ß; synapsin I; synaptophysin.


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