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

• DOI: 10.1093/toxsci/kfl134
• Publication Date: 2006-10-18T03:18:59Z
• Authors: Lidia Strużyńska; Beata Dąbrowska-B...; Katarzyna Koza; Grzegorz Sulkowski
• Keywords: Proinflammatory cytokine; Neurotoxicity; Synapsin I; Forebrain; Synaptophysin; Gliosis

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 in brain tissue. Activation astroglia may often loss the buffering function and contribute pathological processes. This phenomenon is accompanied by death neuronal cells connected with inflammatory events arising from production wide range cytokines chemokines. The effects prolonged exposure Pb upon glial activation examined immature rats investigate potential proinflammatory effect. When analyzed at protein level, observed after exposure, as reflected increased level fibrillary acidic S-100β proteins all parts examined. These changes associated elevation cytokines. Production interleukin (IL)-1β tumor necrosis factor-α hippocampus, IL-6 seen forebrain. expression fractalkine both hippocampus forebrain but inconsiderably cerebellum. In parallel cytokine expression, signs synaptic damage decreased levels axonal markers synapsin I synaptophysin. Obtained results indicate chronic coexisting neurodegenerative features new mechanism rat brain.