Prion infection impairs the cellular response to oxidative stress

The molecular mechanism of neurodegeneration in transmissible spongiform en cephalopathies remains uncertain. In this study, it was demonstrated that p rion-infected hypothalamic neuronal GT1 cells displayed a higher sensitivit y to induced oxidative stress over noninfected cells. In addition, the infe cted 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 indicate s for the first time that prion infection results in an alteration of the m olecular mechanisms promoting cellular resistance to reactive oxygen specie s. This finding is vital for future therapeutic approaches in transmissible spongiform encephalopathies and the understanding of the function of the p rion protein.