SPINAL ISCHEMIA, ITS MECHANISM AND STRATEGY OF TREATMENT-A NEW MODEL AND GLIAL REACTION AND INDUCTION

light and electron microscopic localization of single strand DNA protein，a marker of apoptosis was studied. Immunoreaction was recognized in the nucleus withoutmorphological changes 1 day after ischemic insult. Degradation of single strand DNA can occur duringdelayed neuronal death, preceding the appearance of double strand DNA breaks.（Neurosci Lett 240）69,1998)2) DDC induced apoptosis in a morphological nature in PC12 cells，and led to down -regulation of Cu/Zn-SOD activitythen reduced intracellular H - D22 - D2O - D22 - D2. A hypoxia prevented the cells from DDC-inducedapoptosis. These data confirmed oi D22 induced apoptosis in PC12 cells. Nitro-oxide-synthetase，fechelator did not prevent the apoptosis.Peroxinitrate and also OH did not contribute DDC-inducedapoptosis. NGF和NAC protected the apoptosis. DDC未激活NF-kB. We concluded that NACreduced dpc -induced apoptosis by interception of an unknown direct signal pathwayby which O - 22 - D2 induced apoptosis。

1) The light and electron microscopic localization of single strand DNA protein, a marker of apoptosis was studied. Immunoreaction was recognized in the nucleus without morphological changes 1 day after ischemic insult. Degradation of single strand DNA can occur during delayed neuronal death, preceding the appearance of double strand DNA breaks.(Neurosci Lett 240 : 69, 1998)2) DDC induced apoptosis in a morphological nature in PC12 cells, and led to down -regulation of Cu/Zn-SOD activity, then reduced intracellular HィイD22ィエD2OィイD22ィエD2. A hypoxia prevented the cells from DDC-induced apoptosis. These data confirmed OィイD22ィエD2 induced apoptosis in PC12 cells. Nitro-oxide-synthetase, Fe-chelator did not prevent the apoptosis.Peroxinitrate and also OH did not contribute DDC-induced apoptosis. NGF and NAC protected the apoptosis. DDC did not activate NF-kB. We concluded that NAC reduced DDC-induced apoptosis by interception of an unknown direct signal pathway, by which OィイD22ィエD2 induced apoptosis.