A possible mechanism for PrP^<Sc> formation through modification with a lipid peroxidation product hydroxylnonenal at the membrane interface

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Pathogenesis of prion diseases involves transition of PrP^C into PrP^<Sc>. The purpose of this study was to examine if the lipid peroxidation product, 4-hydroxy nonenal(HNE) would modify the structure of PrP^C through formation of PrP^C-HNE adducts and trigger the formation of insoluble PrP^<Sc>. The mass spectrometry analysis showed that PrP^C was accessible to HNE modification when the cells expressing PrP^Cwere exposed to exogenous HNE. However, the content of proteinase K-resistant PrP bearing HNE adducts was negligible, indicating that HNE modification would not be a sole cause for PrP^<Sc> formation.