Deferoxamine Attenuates Iron-Induced Oxidative Stress and Prevents Mitochondrial Aggregation and α-Synuclein Translocation in SK-N-SH Cells in Culture

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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.