Hydroxyl radicals generated in the rat spinal cord at the level produced by impact injury induce cell death by necrosis and apoptosis: Protection by a metalloporphyrin
Hydroxyl radicals generated in the rat spinal cord at the level produced by impact injury induce cell death by necrosis and apoptosis: Protection by a metalloporphyrin
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DOI:
10.1016/j.neuroscience.2004.03.054
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发表时间:
2004-01-01
期刊:
影响因子:
3.3
通讯作者:
Liu, D
中科院分区:
文献类型:
--
作者:
Bao, F;Liu, D
We previously measured the time courses of hydrogen peroxide (H2O2), hydroxyl radical ((OH)-O-.), and catalytic iron increases following traumatic spinal cord injury (SCI). This study determines whether the SCI-elevated level of (OH)-O-. causes cell death. OH was generated by administering H2O2 and Fe2+ at the concentrations attained following SCI, each through a separate microdialysis fiber inserted laterally into the gray matter of the cord. The duration of (OH)-O-. generation mimics the duration of its elevation after SCI. The death of neurons and astrocytes was characterized at 24 h post-(OH)-O-. exposure and quantitated by counting surviving cells along the fiber track in sections stained with Cresyl Violet, or immunohistochemically stained with anti-neuron-specific enolase (anti-NSE) and anti-glial fibrillary acidic protein (antiGFAP). DNA fragmentation in neurons was characterized by double staining with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling JUNEL) and anti-NSE. Using a one way ANOVA followed by the Tukey test, we demonstrated that (OH)-O-. generated in the cord induced significant losses of neurons in both Cresyl Violet (P