In:
Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 97, No. 25 ( 2000-12-05), p. 13937-13942
Kurzfassung:
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.
Materialart:
Online-Ressource
ISSN:
0027-8424
,
1091-6490
DOI:
10.1073/pnas.250289197
Sprache:
Englisch
Verlag:
Proceedings of the National Academy of Sciences
Publikationsdatum:
2000
ZDB Id:
209104-5
ZDB Id:
1461794-8
SSG:
11
SSG:
12
