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Oxidative Stress Induces Intralysosomal Accumulation of Alzheimer Amyloid β‐Protein in Cultured Neuroblastoma Cells
Author(s) -
ZHENG LIN,
ROBERG KARIN,
JERHAMMAR FREDRIK,
MARCUSSON JAN,
TERMAN ALEXEI
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1354.032
Subject(s) - oxidative stress , hyperoxia , autophagy , extracellular , microbiology and biotechnology , chemistry , senile plaques , pathogenesis , neuroblastoma , amyloid (mycology) , reactive oxygen species , alzheimer's disease , biology , medicine , biochemistry , cell culture , oxygen , immunology , disease , apoptosis , inorganic chemistry , genetics , organic chemistry
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 β‐protein (Aβ). Aβ 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) Aβ‐containing lysosomes, which were not typical of control cells, showing a distinct localization of Aβ 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.