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 -Protein in Cultured Neuroblastoma Cells
a Division of Geriatric Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden b Division of Otorhinolaryngology, Faculty of Health Sciences, Linköping University, Linköping, Sweden c Division of Experimental Pathology, Faculty of Health Sciences, Linköping University, Linköping, Sweden
Key Words: Alzheimer disease • amyloid  -protein • autophagy • lysosomes • oxidative stress
Address for correspondence: Lin Zheng, Division of Geriatric Medicine, Faculty of Health Sciences, Linköping University, SE-58185 Linköping, Sweden. Voice: +46-13-222271; fax: +46-13-221529. e-mail: linzh{at}inr.liu.se
Oxidative stress is considered important for the pathogenesis of Alzheimer's disease (AD), which is characterized by the formation of extracellular senile plaques, mainly composed of amyloid
-protein (A). A also accumulates within AD neurons and is believed to exert cellular toxicity through lysosomal labilization. We report that the exposure of human neuroblastoma cells to hyperoxia (40% vs. 8% ambient oxygen) induced the accumulation of large (over 1 µM) A-containing lysosomes, which were not typical of control cells, showing a distinct localization of A and lysosomal markers. An inhibitor of autophagy, 3-methyladenine, suppressed the effect of hyperoxia. The results suggest a link between the involvement of oxidative stress and lysosomes in AD.
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