Abstract
Reactive oxygen species (ROS) attack several living organs and induce neuronal cell death. Previously, we found that treatment with a low concentration of hydrogen peroxide induced neurite degeneration prior to the cell death. The neurites showed abnormal morphologies including beads formation, shrinkage and fragmentation. This phenomenon also observed in hippocampus of the normal-aged and vitamin E-deficient mice. In order to clarify the mechanism of neurite degeneration, we measured lipid peroxidative products in hydrogen peroxide-treated cells. The LOOH levels were significantly increased compared to the untreated group. If cell membranes are oxidized by ROS, large parts of receptors and ion channels may be also damaged. Here, we show the elucidation of the relationship between calcium influx and neurite degeneration in cultured neurons. Treatment with an ionomycin (calcium ionophore) induced neuronal cell death in a concentration- and a time-dependent manner. Treatment with a low concentration of ionomycin induced neurite degeneration via influx of calcium ions, mitochondrial-dependent superoxide production and mitochondrial membrane oxidations. These phenomena were recorded by a time-lapse live imaging system. Finally, these neurite degeneration prevented by antioxidant vita.
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