The Mechanism of Cell Death during Hypoxia

许多研究表明，脂质过氧化和其他氧化剂发生在缺血再灌注损伤中。然而，氧化是否发生在缺血或再灌注阶段尚不清楚。本研究以小鼠胚胎成纤维细胞（MEFs）为实验对象，观察在缺血（再灌注或缺氧再氧化）过程中氧化剂的发生方式和时间。用电子传递系统的抗氧化剂或抑制剂对细胞进行处理，观察脂质过氧化的机制。用荧光染料检测脂质过氧化和戴尔损伤。结果，缺血期细胞死亡，再灌注后死亡的细胞占63.9%。KCN可抑制细胞死亡。抗真菌素和粘噻唑可抑制缺血时的细胞死亡，再灌注时的细胞死亡无抑制作用。脂质过氧化在缺血时检测到，而在再灌注时没有检测到，并且KCN可以抑制脂质过氧化，而抗星酸A、粘氧噻唑和鱼藤酮则没有。结果表明，再灌注时不发生脂质过氧化，而缺血时发生脂质过氧化，KCN可抑制缺血时细胞死亡和脂质过氧化。

Many reseaithers indicate that lipid peroxidation and other oxidants occur in dell damage during ischemia-reperfusion. However it is still not clear that whether oxidants occur during ischemia or reperfusion phase. In this study, mouse emdryonic fibroblasts (MEFs) were used for experiment, to see how and when the oxidants occur during ischemia (reperfusion, or hypoxia and reoxygenation.). Some antioxidants or inhibitors of electron transfer system were treated for the cells to see the mechanism of lipid peroxidation. We used fluorescent dyes to detect the lipid peroxidation and dell damage. As a result, cell death occurs from ischemia pahase, and 63.9% cells were dead after reperfusion. Cell death was inhibited by KCN. Cell death during ischemia was inhibited by antimycinAor myxothiazol, and that during reperfusion was not inhibited by them. Lipid peroxidation was detected during ischemia and not during reperfusion, and it was inhibited by KCN and was not by antimacin A, myxotiazol or rotenone. From these results it was indicated that lipid peroxidation did not cccur during reperfusion but did during ischemia, and KCN could inhibit cell death and lipid peroxidation during ischemia.