Prion Infection Impairs the Cellular Response to Oxidative Stress

The molecular mechanism of neurodegeneration in transmissible spongiform encephalopathies remains uncertain. In this study, it was demonstrated that prion-infected hypothalamic neuronal GT1 cells displayed a higher sensitivity to induced oxidative stress over noninfected cells. In addition, the infe...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2000-12, Vol.97 (25), p.13937-13942
Main Authors: Milhavet, O, McMahon, H E, Rachidi, W, Nishida, N, Katamine, S, Mangé, A, Arlotto, M, Casanova, D, Riondel, J, Favier, A, Lehmann, S
Format: Article
Language:English
Subjects:
Antibodies
Biological Sciences
Blotting, Western
Cell Line
Cell lines
DNA Fragmentation
Enzymes
Glutathione - metabolism
GT1 cells
Infections
Lipid Peroxidation
Neurology
Neurons
Oxidative Stress
Prion diseases
Prion Diseases - pathology
Prions
Proteins
Spongiform encephalopathies
Superoxide Dismutase - metabolism
Superoxides
Viability
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Summary:The molecular mechanism of neurodegeneration in transmissible spongiform encephalopathies remains uncertain. In this study, it was demonstrated that prion-infected hypothalamic neuronal GT1 cells displayed a higher sensitivity to induced oxidative stress over noninfected cells. In addition, the infected cells presented an increased lipid peroxidation and signs of apoptosis associated with a dramatic reduction in the activities of the glutathione-dependent and superoxide dismutase antioxidant systems. This study indicates for the first time that prion infection results in an alteration of the molecular mechanisms promoting cellular resistance to reactive oxygen species. This finding is vital for future therapeutic approaches in transmissible spongiform encephalopathies and the understanding of the function of the prion protein.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.250289197