MECHANISMS OF OXIDATIVE INJURY IN NEURONS AND ASTROCYTES

缺氧和高氧降低脱氢酶(LDH)和蛋白质 内容物，引起细胞水肿，并破坏原代细胞的细胞膜 星形胶质细胞的培养。1，6-二磷酸果糖(FDP)+葡萄糖 (GLC)可防止这些变化，但仅有FDP或GLC不能。 缺氧时，FDP+使Na+-K+-ATP酶活性升高 GLC存在；单独使用GLC或FDP可降低GLC。我们假设 FDP的保护作用要么是由于增加了 正常细胞内离子平衡的代谢与维持 或对氧自由基的产生和细胞膜的影响 毁灭。为了检验我们的假设，我们将确定 FDP增加低氧和低氧大鼠的代谢和ATP含量 高氧性星形胶质细胞和神经元，FDP是否维持正常 细胞内离子浓度，FDP是否阻止细胞 水肿，以及FDP是否保持膜完整性和 功能。要确定FDP是否可以防止 氧自由基对常氧和高氧细胞的影响，我们将 确定氧自由基的产生是否增加， 膜是否改变。膜脂肪酸组成 也将被确定。这些研究将提供新的 关于低氧和高氧对人体健康影响的信息 星形胶质细胞和神经元以及FDP的作用机制 防止低氧和高氧的有害影响。这 信息将增加我们对细胞是如何 被异常的氧气状态伤害，并可能导致新的方法 对大脑的保护。

Hypoxia and hyperoxia decrease dehydrogenase (LDH) and protein content, cause cell edema, and disrupt cell membranes of primary cultures of astrocytes. Fructose-1, 6-diphosphate (FDP) + glucose (GLc) prevents these changes, but FDP or Glc alone does not. During hypoxia, Na+-K+ ATP-ase activity increases when FDP + Glc is present; it decreases with Glc or FDP alone. We postulate that the protective effects of FDP are either due to increased metabolism and maintenance of normal cellular ion homeostasis or to effects on oxygen free radical production and cell membrane destruction. To test our hypotheses, we will determine whether FDP increases metabolism and ATP content of hypoxic and hyperoxic astrocytes and neurons, whether FDP maintains normal intracellular concentrations of ions, whether FDP prevents cell edema, and whether FDP maintains membrane integrity and function. To determine whether FDP prevents the effects of oxygen free radicals on normoxic and hyperoxic cells, we will determine whether oxygen free radical production increases, whether membrane is altered. Membrane fatty acid composition will also be determined. These studies will provide new information about the effects of hypoxia and hyperoxia on astrocytes and neurons and about the mechanism by which FDP prevents detrimental effects of low and high oxygen. This information will increase our understanding of how cells are injured by abnormal oxygen states and may lead to new methods of brain protection.