P. SangchotS. SharmaB. ChetsawangJ. PorterP. GovitrapongManuchair EbadiUND School of Medicine & Health Sciences - Northeast CampusMahidol UniversityUniversity of North Dakota2018-07-242018-07-242002-12-01Developmental Neuroscience. Vol.24, No.2-3 (2002), 143-153037858662-s2.0-0036970672https://repository.li.mahidol.ac.th/handle/123456789/20594One 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.Mahidol UniversityNeuroscienceArticleSCOPUS10.1159/000065700