Abstract
We investigated the influence of reactive oxygen species and free radicals on axonal transport in cultured mouse dorsal root ganglion neurons. Video-microscopy was used for observation of movement of organelles. The nitric oxide (NO) donor NOC18 (100 μM) and the hydrogen peroxide (H2O2) donor tert-butyl hydroperoxide (100 μM) significantly decreased anterograde and retrograde axonal transport of organelles. High concentration (1 mM) of tert-butyl hydroperoxide immediately induced swelling of mitochondria and cell death. The superoxide dismutase (SOD) inhibitor diethyldithio carbamate (100 μM) significantly decreased anterograde and retrograde axonal transport. High concentration (10 mM) of diethyl carbamate induced swelling of growth cones and vacuole formation in the cell body. The singlet oxygen scavengers L-ascorbic acid (25 mM) and L-histidine (10 mM) and the NO scavenger PTIO (30 μM) slightly but significantly increased axonal transport. In contrast, the hydroxyl radical scavenger dimethyl thioirea (5 mM) had no effect. These results indicate that exogenous and endogenous reactive oxygen species and free radicals impair axonal transport. This may lead to irreversible axonal degeneration and neuronal cell death, which are observed in neurodegenerative diseases. [J Physiol Sci. 2007;57 Suppl:S130]
