Neuro-inflammatory response in rats chronically exposed to (137)Cesium

After the Chernobyl nuclear accident, behavioural disorders and central nervous system diseases were frequently observed in populations living in the areas contaminated by (137)Cs. Until now, these neurological disturbances were not elucidated, but the presence of a neuro-inflammatory response could...

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Veröffentlicht in:Neurotoxicology (Park Forest South) 2008-03, Vol.29 (2), p.343
Hauptverfasser: Lestaevel, Philippe, Grandcolas, Line, Paquet, François, Voisin, Philippe, Aigueperse, Jocelyne, Gourmelon, Patrick
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container_issue 2
container_start_page 343
container_title Neurotoxicology (Park Forest South)
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creator Lestaevel, Philippe
Grandcolas, Line
Paquet, François
Voisin, Philippe
Aigueperse, Jocelyne
Gourmelon, Patrick
description After the Chernobyl nuclear accident, behavioural disorders and central nervous system diseases were frequently observed in populations living in the areas contaminated by (137)Cs. Until now, these neurological disturbances were not elucidated, but the presence of a neuro-inflammatory response could be one explanation. Rats were exposed for 3 months to drinking water contaminated with (137)Cs at a dose of 400Bqkg(-1), which is similar to that ingested by the population living in contaminated areas in the former USSR countries. Pro-inflammatory and anti-inflammatory cytokine genes were assessed by real-time PCR in the frontal cortex and the hippocampus. At this level of exposure, gene expression of TNF-alpha and IL-6 increased in the hippocampus and gene expression of IL-10 increased in the frontal cortex. Concentration of TNF-alpha, measured by ELISA assays, was also increased in the hippocampus. The central NO-ergic pathway was also studied: iNOS gene expression and cNOS activity were significantly increased in the hippocampus. In conclusion, this study showed for the first time that sub-chronic exposure with post-accidental doses of (137)Cs leads to molecular modifications of pro- and anti-inflammatory cytokines and NO-ergic pathway in the brain. This neuro-inflammatory response could contribute to the electrophysiological and biochemical alterations observed after chronic exposure to (137)Cs.
doi_str_mv 10.1016/j.neuro.2008.01.001
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subjects Animals
Cesium Radioisotopes - toxicity
Chernobyl Nuclear Accident
Cytokines - genetics
Cytokines - metabolism
Enzyme Induction
Enzyme-Linked Immunosorbent Assay
Frontal Lobe - enzymology
Frontal Lobe - metabolism
Frontal Lobe - radiation effects
Gene Expression - radiation effects
Hippocampus - enzymology
Hippocampus - metabolism
Hippocampus - radiation effects
Interleukin-10 - metabolism
Interleukin-1beta - metabolism
Interleukin-6 - metabolism
Interleukin-8 - metabolism
Male
Neuritis - etiology
Neuritis - genetics
Neuritis - metabolism
Nitric Oxide Synthase Type II - biosynthesis
Nitric Oxide Synthase Type II - genetics
Nitric Oxide Synthase Type III
Polymerase Chain Reaction
Rats
Rats, Sprague-Dawley
RNA, Messenger - metabolism
Transforming Growth Factor beta - metabolism
Tumor Necrosis Factor-alpha - metabolism
Up-Regulation
title Neuro-inflammatory response in rats chronically exposed to (137)Cesium
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