Abstract
Alzheimer's disease (AD) is the most common form of dementia. It is characterized by aggregation of amyloid plaques and neurofibrillary tangles. The neurotoxic action of amyloid β-peptide (Aβ) involves formation of reactive oxygen species. Trans fatty acids (TFAs) are not only exogenously derived from dietary food, but also endogenously formed by free radicals. Thus, we utilized the PC-12 cell model to investigate the correlation between radical stress and endogenous formed TFAs. The results showed that thiyl radicals significantly increased TFA formation in PC-12 cells in both pre-treatment and co-treatment experiments. It was also found that retinol acetate significantly decreased thiyl radical-catalysed TFA formation in PC-12 cells. The anti-isomerization activity of retinol acetate resulted, at least in part, from its high absorption efficiency by PC-12 cells and its thiyl radical scavenging activity. Therefore, retinol acetate may serve as a potential antioxidant for functional foods against TFA formation during pathogenesis of AD.
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