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| SUPEROXIDE-DISMUTASE DELAYS NEURONAL APOPTOSIS - A ROLE FOR REACTIVE OXYGEN SPECIES IN PROGRAMMED NEURONAL DEATH |
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| Author(s): GREENLUND LJS, DECKWERTH TL, JOHNSON EM |
| Source: NEURON Volume: 14 Issue: 2 Pages: 303-315 Published: FEB 1995 |
| Times Cited: 591 References: 56 |
| Abstract: Sympathetic neurons in culture die by apoptosis when deprived of nerve growth factor (NGF). We used this model of programmed cell death to study the mechanisms that mediate neuronal apoptosis. Cultured sympathetic neurons were injected with copper/zinc superoxide dismutase protein (SOD) or with an expression vector containing an SOD cDNA. In both cases apoptosis was delayed when the neurons were deprived of NGF. The delay was similar to that seen when a bcl-2 expression vector was injected. SOD, injected 8 hr after NGF deprivation, provided no protection, indicating that superoxide production may occur early in response to trophic factor deprivation. We have demonstrated, with a redox sensitive dye, an increase in reactive oxygen species (ROS) that peaked at 3 hr after sympathetic neurons were deprived of NGF. If NGF was added back to the culture medium after the period of peak ROS generation, apoptosis was completely prevented, suggesting that ROS production serves as an early signal, rather than a toxic agent, to mediate apoptosis. |
| Document Type: Article |
| Language: English |
| Reprint Address: GREENLUND, LJS (reprint author), WASHINGTON UNIV, SCH MED, DEPT NEUROL, ST LOUIS, MO 63110 USA |
Addresses:
1. WASHINGTON UNIV, SCH MED, DEPT MOLEC BIOL & PHARMACOL, ST LOUIS, MO 63110 USA |
| Publisher: CELL PRESS, 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 |
| Subject Category: Neurosciences |
| IDS Number: QH294 |
| ISSN: 0896-6273 |
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