Publication: Deferoxamine attenuates iron-induced oxidative stress and prevents mitochondrial aggregation and α-synuclein translocation in SK-N-SH cells in culture
Issued Date
2002-12-01
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ISSN
03785866
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2-s2.0-0036970672
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Mahidol University
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SCOPUS
Bibliographic Citation
Developmental Neuroscience. Vol.24, No.2-3 (2002), 143-153
Suggested Citation
P. Sangchot, S. Sharma, B. Chetsawang, J. Porter, P. Govitrapong, Manuchair Ebadi Deferoxamine attenuates iron-induced oxidative stress and prevents mitochondrial aggregation and α-synuclein translocation in SK-N-SH cells in culture. Developmental Neuroscience. Vol.24, No.2-3 (2002), 143-153. doi:10.1159/000065700 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/20594
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Title
Deferoxamine attenuates iron-induced oxidative stress and prevents mitochondrial aggregation and α-synuclein translocation in SK-N-SH cells in culture
Abstract
One of the defining characteristics of neurodegenerative diseases, including Parkinson's disease, is an abnormal accumulation of iron in the affected brain areas. By using SK-N-SH, a dopaminergic cell line, we have found that iron (100-250 μM FeSO4) decreased cell viability, increased lipid peroxidation, and the said effects were blocked by deferoxamine (DFO: 10 μM). Furthermore, DFO, in the absence of iron, enhanced the level of adenosine triphosphate (ATP), but caused chromatin condensation and cell death. Morphological studies revealed that iron (50-100 μM) altered mitochondrial morphology, disrupted nuclear membrane, and translocated α-synuclein from perinuclear region into the disrupted nucleus. The results of these studies suggest that DFO is able to block and attenuate iron-mediated oxidative stress. However, in the absence of excess iron, DFO itself may have deleterious effects on the morphology and hence integrity of dopaminergic neurons. Copyright © 2002 S. Karger AG, Basel.