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Evidence of oxidative stress in young and aged DJ‐1‐deficient mice
Author(s) -
Raman Arjun V.,
Chou Vivian P.,
Atienza-Duyanen Jennifer,
Di Monte Donato A.,
Bellinger Frederick P.,
Manning-Boğ Amy B.
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.04.001
Subject(s) - oxidative stress , medicine , dopamine , endocrinology , genetically modified mouse , pathogenesis , wild type , midbrain , substantia nigra , transgene , biology , dopaminergic , central nervous system , biochemistry , gene , mutant
Loss of DJ‐1 function contributes to pathogenesis in Parkinson's disease. Here, we investigate the impact of aging and DJ‐1 deficiency in transgenic mice. Ventral midbrain from young DJ‐1‐deficient mice revealed no change in 4‐hydroxy‐2‐nonenal (4‐HNE), but HSP60, HSP40 and striatal dopamine turnover were significantly elevated compared to wildtype. In aged mice, the chaperone response observed in wildtype animals was absent from DJ‐1‐deficient transgenics, and nigral 4‐HNE immunoreactivity was enhanced. These changes were concomitant with increased striatal dopamine levels and uptake. Thus, increased oxidants and diminished protein quality control may contribute to nigral oxidative damage with aging in the model.