The morphological and biochemical changes that occur during chemical hypoxic injury in a neural cell line were studied in the presence and absence of calcium. Oligodendroglial-glioma hybrid cells (ROC-1) were subjected to inhibitors of glycolytic and oxidative ATP synthesis (chemical hypoxia). Complete respiratory inhibition depleted [ATP] to less than 5% of control by 4 min. Blebs appeared on the cell surfaces and cells began to swell within a few minutes of ATP depletion. A 200% increase in cell volume and bleb coalescence preceded irreversible cell injury (lactate dehydrogenase release) which began at approximately 20 min with 50% cell death by 40 min. In energized cells an equivalent degree of osmotic swelling induced by ouabain inhibition of the Na+, K(+)-ATPase pump did not produce blebbing or cell death. Partial inhibition of respiration decreased [ATP] to approximately 10% of control by 40 min. Blebbing and swelling began at 40 min and bleb coalescence preceded plasma membrane disruption which began at approximately 55 min. ATP depletion, blebbing, swelling, and death followed similar time courses in the presence or absence of extracellular calcium ([Ca2+]e). Intracellular calcium ([Ca2+]i) was measured using fura-2. In calcium-containing medium metabolic inhibition caused a transient increase in resting [Ca2+]i (100 +/- 17 nM) followed by a low steady-state level preceding plasma membrane disruption. Following deenergization in calcium-free medium, [Ca2+]i remained below 60 nM throughout injury and death. These data suggest that decreased ATP initiates a sequence of events including bleb formation and cell swelling that lead to irreversible cell injury in the absence of large increases in [Ca2+]i.

译文

:研究了在有钙和无钙的情况下,神经细胞系在化学性低氧损伤过程中发生的形态和生化变化。少突胶质细胞-神经胶质瘤杂交细胞(ROC-1)受到糖酵解和氧化ATP合成的抑制剂(化学性缺氧)。到4分钟时,完全的呼吸抑制作用使[ATP]减少至控制量的5%以下。小球出现在细胞表面,并且在ATP耗尽的几分钟内细胞开始肿胀。细胞体积增加200%和气泡合并之前发生不可逆的细胞损伤(乳酸脱氢酶释放),这种损伤始于约20分钟,到40分钟时细胞死亡50%。在通电的细胞中,哇巴因对Na,K()-ATPase泵的抑制作用引起的同等程度的渗透性溶胀不会产生起泡或细胞死亡。到40分钟,对呼吸的部分抑制使[ATP]降至对照的约10%。起泡和溶胀在40分钟开始,起泡聚结在质膜破裂之前发生,其在约55分钟开始。在存在或不存在细胞外钙([Ca2] e)的情况下,ATP的消耗,起泡,膨胀和死亡也遵循相似的时间过程。使用呋喃2测定细胞内钙([Ca2] i)。在含钙的培养基中,代谢抑制导致静止的[Ca2] i(100 /-17 nM)短暂增加,随后在质膜破裂之前处于低稳态水平。在无钙培养基中断电后,[Ca2] i在整个伤害和死亡中均保持在60 nM以下。这些数据表明,降低的ATP会引发一系列事件,包括气泡形成和细胞肿胀,在[Ca2] i没有大幅增加的情况下会导致不可逆的细胞损伤。

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