Different pattern of brain pro-/anti-oxidant activity between depleted and enriched uranium in chronically exposed rats
| Autor: | Isabelle Dublineau, Patrick Gourmelon, H. Ben Soussan, Philippe Lestaevel, P. Voisin, B. Dhieux, E. Romero, H. Berradi |
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| Přispěvatelé: | Radiobiologie et épidémiologie (DRPH/SRBE), Institut de Radioprotection et de Sûreté Nucléaire (IRSN) |
| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
Time Factors
Antioxidant antioxidant medicine.medical_treatment [SDV]Life Sciences [q-bio] Administration Oral antioxidant activity Toxicology medicine.disease_cause Antioxidants Rats Sprague-Dawley Lipid peroxidation chemistry.chemical_compound 0302 clinical medicine neurotoxicity oxidative stress rat glutathione peroxidase Cerebral Cortex chemistry.chemical_classification 0303 health sciences biology Reverse Transcriptase Polymerase Chain Reaction messenger RNA Glutathione peroxidase catalase article lipid peroxidation superoxide dismutase ceruloplasmin enzyme activity natural resistance associated macrophage protein 2 Biochemistry priority journal Catalase uranyl nitrate Environmental Pollutants medicine.medical_specialty brain animal experiment Drinking animal tissue brain cortex Superoxide dismutase uranium 03 medical and health sciences male lipid nitric oxide Internal medicine medicine Animals controlled study defense mechanism 030304 developmental biology Reactive oxygen species nonhuman Rattus drinking water ferritin Neurotoxicity medicine.disease radiology Rats Endocrinology chemistry Ferritins biology.protein gene expression protein 030217 neurology & neurosurgery Oxidative stress |
| Zdroj: | Toxicology Toxicology, 2009, 258 (1), pp.1-9. ⟨10.1016/j.tox.2008.12.021⟩ |
| DOI: | 10.1016/j.tox.2008.12.021⟩ |
| Popis: | Uranium is not only a heavy metal but also an alpha particle emitter. The main toxicity of uranium is expected to be due to chemiotoxicity rather than to radiotoxicity. Some studies have demonstrated that uranium induced some neurological disturbances, but without clear explanations. A possible mechanism of this neurotoxicity could be the oxidative stress induced by reactive oxygen species imbalance. The aim of the present study was to determine whether a chronic ingestion of uranium induced anti-oxidative defence mechanisms in the brain of rats. Rats received depleted (DU) or 4% enriched (EU) uranyl nitrate in the drinking water at 2 mg-1 kg-1 day-1 for 9 months. Cerebral cortex analyses were made by measuring mRNA and protein levels and enzymatic activities. Lipid peroxidation, an oxidative stress marker, was significantly enhanced after EU exposure, but not after DU. The gene expression or activity of the main antioxidant enzymes, i.e. superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), increased significantly after chronic exposure to DU. On the contrary, oral EU administration induced a decrease of these antioxidant enzymes. The NO-ergic pathway was almost not perturbed by DU or EU exposure. Finally, DU exposure increased significantly the transporters (Divalent-Metal-Transporter1; DMT1), the storage molecule (ferritin) and the ferroxidase enzyme (ceruloplasmin), but not EU. These results illustrate that oxidative stress plays a key role in the mechanism of uranium neurotoxicity. They showed that chronic exposure to DU, but not EU, seems to induce an increase of several antioxidant agents in order to counteract the oxidative stress. Finally, these results demonstrate the importance of the double toxicity, chemical and radiological, of uranium. © 2009 Elsevier Ireland Ltd. All rights reserved. |
| Databáze: | OpenAIRE |
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