Mitochondrial dysfunction induced by oxidative stress in the brains of hamsters infected with the 263 K scrapie agent
| Autor: | Yong-Sun Kim, Seung Il Choi, Won-Kyu Ju, Richard I. Carp, Eun-Kyoung Choi, Jin Kim, Henry M . Wisniewski, Ho-Zoo Lea |
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| Rok vydání: | 1998 |
| Předmět: |
medicine.medical_specialty
Glutathione reductase Scrapie Mitochondrion Biology medicine.disease_cause Antioxidants Pathology and Forensic Medicine Prion Diseases Lipid peroxidation Electron Transport Complex IV Cellular and Molecular Neuroscience chemistry.chemical_compound Cytosol Internal medicine Cricetinae medicine Animals chemistry.chemical_classification Adenosine Triphosphatases Glutathione Peroxidase Superoxide Dismutase Glutathione peroxidase Neurodegeneration Brain medicine.disease Catalase Mitochondria Enzyme Activation Microscopy Electron Oxidative Stress Endocrinology medicine.anatomical_structure Glutathione Reductase chemistry Cerebral cortex Immunology Female Neurology (clinical) Lipid Peroxidation Reactive Oxygen Species Oxidative stress |
| Zdroj: | Acta neuropathologica. 96(3) |
| ISSN: | 0001-6322 |
| Popis: | Scrapie, one of the prion diseases, is a transmissible neurodegenerative disease of sheep and other animals. Clinical symptoms of prion diseases are characterized by a long latent period, followed by progressive ataxia, tremor, and death. To study the induction of neurodegeneration during scrapie infection, we have analyzed the activities of various antioxidant enzymes and mitochondrial enzymes in cerebral cortex, brain stem, and cerebellum of scrapie-infected hamsters. The activity of mitochondrial Mn-superoxide dismutase (SOD) was decreased, while the activities of cytosolic Cu/Zn-SOD and catalase were not altered in infected brains. The activities of glutathione peroxidase and glutathione reductase were increased in scrapie-infected hamsters. The decreased activity of Mn-SOD might result in increasing oxidative stress in the mitochondria of infected brain; this concept is supported by our findings of a high level of lipid peroxidation, and low levels of ATPase and cytochrome c oxidase activity in the infected cerebral mitochondria. In addition, structural abnormalities of mitochondria have been observed in the neurons of hippocampus and cerebral cortex of infected brain. These results suggest that mitochondrial dysfunction caused by oxidative stress gives rise to neurodegeneration in prion disease. |
| Databáze: | OpenAIRE |
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