Résumé
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.