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- Title
Distinct Mechanisms Account forβ-Amyloid Toxicity in PC12 and Differentiated PC12 Neuronal Cells.
- Authors
Yen-Jen Sung; Chia-Io Cheng; Chaio-Sung Chen; Hsien-Bin Huang; Fong-Lee Huang; Pei-Chun Wu; Ming-Shi Shiao; Huey-Jen Tsay
- Abstract
Whether reactive oxygen species (ROS) mediate β-amyloid (Aβ) neurotoxicity remains controversial. Naive PC12 cells (PC12) and nerve growth factor-differentiated PC12 cells (dPC12) were used to study the role of ROS in cell death induced by Aβ[sub25-35]. The viability of PC12 and dPC12 cells decreased by 30-40% after a 48-hour exposure to 20 μM Aβ[sub25-35]. Microscopic examination showed that Aβ[sub25-35] induced necrosis in PC12 cells and apoptosis in dPC12 cells. Vitamin E (100 μM) and other antioxidants protected PC12 cells, but not dPC12 cells, against the cytotoxic effect of Aβ[sub25-35]. Since H[sub2]O[sub2] has been proposed to be involved in Aβ toxicity, the effects of H[sub2]O[sub2] on PC12 and dPC12 cells were studied. Differentiated PC12 cells appeared to be significantly more resistant to H[sub2]O[sub2] than naive PC12 cells. These data suggest that ROS may mediate Aβ[sub25-35} toxicity in PC12 cells but not in dPC12 cells. Because the intracellular levels of ROS were elevated during the differentiation of PC12 cells, the baseline levels of ROS in these two model cell types may determine the intracellular mediators for Aβ[sub25-35] toxicity. Therefore, the protective effects of antioxidants against Aβ may depend upon the redox state of the cells.
- Subjects
AMYLOID beta-protein; NEUROTOXICOLOGY; CELLS; OXYGEN; ANTIOXIDANTS
- Publication
Journal of Biomedical Science, 2003, Vol 10, Issue 4, p379
- ISSN
1021-7770
- Publication type
Article
- DOI
10.1007/BF02256429