Lipid peroxidation during ischemia depends on ischemia time in warm ischemia and reperfusion of rat liver
Lipid peroxidation during ischemia depends on ischemia time in warm ischemia and reperfusion of rat liver
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DOI：
10.1016/j.freeradbiomed.2005.02.004
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发表时间：
2005-05-15
影响因子：
7.4
通讯作者：
Todo, S
中科院分区：
文献类型：
--
作者：
Fukai, M;Hayashi, T;Todo, S
长时间的肝脏热缺血与再灌注后的氧化应激有关。然而，缺血期间氧化应激的程度一直存在争议。本研究的目的是阐明缺血期间脂质过氧化是否进展，并阐明缺血期间的氧化应激是否加剧再灌注后的氧化损伤。使大鼠单独经历30至120分钟的70%热缺血或随后再灌注60分钟。通过作为主要 LPO 产物的氢过氧化磷脂酰胆碱 (PC-OOH) 和氢过氧化磷脂酰乙醇胺 (PE-OOH) 的量来评估脂质过氧化 (LPO)。还测定了由氢过氧化物降解的丙二醛和 4-羟基-2-壬烯醛 (MDA + 4-HNE) 的总量。 PC-OOH 和 PE-OOH 在缺血 60 和 120 分钟时显着增加，同时氧化型谷胱甘肽也增加。这些氢过氧化物在60分钟缺血后60分钟再灌注时没有增加，而在120分钟缺血后60分钟再灌注时，随着磷脂氢过氧化物谷胱甘肽过氧化物酶和超氧化物歧化酶的失活，它们确实增加。 MDA + 4-HNE 的量表现出类似的变化，但随着缺血时间超过 60 分钟，产生速度下降。总之，氧化应激在缺血期间进展并引发再灌注后的氧化损伤。次级 LPO 产品敏感性较低，尤其是在缺血期间，这可能导致可能的低估和差异。 (c) 2005 Elsevier Inc. 保留所有权利。
Prolonged hepatic warm ischemia has been incriminated in oxidative stress after reperfusion. However, the magnitude of oxidative stress during ischemia has been controversial. The aims of the present study were to elucidate whether lipid peroxidation progressed during ischemia and to clarify whether oxidative stress during ischemia aggravated the oxidative damage after reperfusion. Rats were subjected to 30 to 120 min of 70% warm ischemia alone or followed by reperfusion for 60 min. Lipid peroxidation (LPO) was evaluated by amounts of phosphatidylcholine hydroperoxide (PC-OOH) and phosphatidylethanolamine hydroperoxide (PE-OOH) as primary LPO products. Total amounts of malondialdehyde and 4-hydroxy-2-nonenal (MDA + 4-HNE), degraded from hydroperoxides, were also determined. PC-OOH and PE-OOH significantly increased at 60 and 120 min ischemia with concomitant increase of oxidized glutathione. These hydroperoxides did not increase at 60 min reperfusion after 60 min ischemia, whereas they did increase at 60 min reperfusion after 120 min ischemia with deactivation of phospholipid hydroperoxide glutathione peroxidase and superoxide dismutase. The amount of MDA + 4-HNE exhibited similar changes, but the velocity of production dropped with ischemic time longer than 60 min. In conclusion, oxidative stress progressed during ischemia and triggered the oxidative injury after reperfusion. Secondary LPO products are less sensitive, especially during ischemia, which may cause possible underestimation and discrepancy. (c) 2005 Elsevier Inc. All rights reserved.