NR ATNJ
AU Martin,S.F.; Castilla,J.; Brun,A.; Salguero,F.J.; Villalba,J.M.; Torres,J.M.
TI CoQ and protein/lipid oxidation in BSE inoculated Bo-PrP-Tg Mice
QU International Conference - Prion 2005: Between fundamentals and society's needs - 19.10.-21.10.2005, Congress Center Düsseldorf - Poster Session: Human prions, risk of blood products, and therapy HUMAN-07
PT Konferenz-Poster
AB Oxidative stress and antioxidants play an important role in the neurodegenerative diseases. However, the exact participation of oxidative stress and antioxidants in prion diseases are still unknown in prion diseases. Here, we have evaluated levels of coenzyme Q (CoQ), an important endogenous lipophilic antioxidant, as well as the antioxidant/prooxidant status of brain tissues by measuring oxidative damage in proteins and lipids after intra-cerebral BSE infection in Bo-PrPc6OR transgenic mice (Castilla et al., Arch. Virol 148, 2003). Our results indicated that the ratio between the two CoQ homologues that are present in mice (CoQ9 and CoQ10) did not experience any change during the evolution of the illness. However, significant increases in total CoQ9 and CoQ10 were observed in BSE-inoculated mice 150 days after inoculation in comparison with control mice. This increase was coincident with the exhibition of the first neuropathological alterations (vacuolization, astrogliosis,...) and PrPres deposition in nervous tissues. In addition, differences in CoQ9 and CoQ10 levels, neuropathological alterations and PrPres deposition in nervous tissues were further increased during the evolution of the illness. On the other hand, oxidation of lipids, proteins and picnosis in hypothalamus were only observed in the final phase of the illness. These observations were also confirmed in samples of brains from dead animals inoculated with a low titer BSE inoculum (400-600 days post-inoculation). Our results suggest that CoQ9 and CoQ10-dependent antioxidant systems are upregulated in response to increased oxidative stress induced by BSE in the nervous tissues. Whereas induction of these endogenous antioxidant systems may be insufficient to prevent the development of the illness, our results open a new research line to understand the possible use of antioxidant as therapy against prion diseases.
AD Sergio F. Martín, Joaquin Castilla, Alejandro Brun, Francisco J. Salguero, Juan M. Torres, Centro de Investigación en Sanidad Animal (CISA-INIA), Spain; Jose M. Villalba, Universidad de Córdoba, Spain
SP englisch
PO Deutschland