Time-dependent inhibition of oxygen radical induced lung injury.
Time-dependent inhibition of oxygen radical induced lung injury.
复制标题
氧自由基引起的肺损伤的时间依赖性抑制。
DOI：
10.1007/bf00914272
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发表时间：
1990
期刊：
影响因子：
5.1
通讯作者：
Johnson,KJ
中科院分区：
文献类型：
--
作者：
Gannon,DE;He,XM;Ward,PA;Varani,J;Johnson,KJ
抗氧化酶过氧化氢酶和超氧化物歧化酶（SOD）可抑制氧代谢产物介导的实验性急性肺损伤。然而，这些酶必须存在以引起保护的具体时间间隔并没有很好地定义。使用两种氧化剂依赖性急性肺损伤的实验模型，一种涉及葡萄糖，葡萄糖氧化酶和乳过氧化物酶的intrichelheal注射和其他涉及眼镜蛇毒因子（CVF）的静脉注射，我们调查了延迟抗氧化剂给药对炎症反应的结果的影响。在这两种情况下，过氧化氢酶和超氧化物歧化酶的保护作用迅速衰减时，他们的管理是一个很短的时间内延迟。例如，当与葡萄糖氧化酶和乳过氧化物酶同时给予时，静脉内过氧化氢酶导致98%的保护，但当过氧化氢酶延迟4分钟时，仅13%的保护。同样，在CVF诱导的肺损伤模型中，当与CVF同时给予时，静脉内过氧化氢酶导致40%的保护，但当过氧化氢酶延迟20分钟时，仅2%的保护，即使损伤的高峰出现在损伤开始后数小时。SOD也有类似的时间依赖性。这些结果表明，在氧自由基介导的急性肺损伤的早期需要抗氧化治疗以有效保护。
Experimental acute lung injury mediated by reactive metabolites of oxygen can be inhibited by the antioxidant enzymes catalase and Superoxide dismutase (SOD). However, the specific time interval during which these enzymes must be present in order to cause protection is not well defined. Using two experimental models of oxidant-dependent acute lung injury, one involving the intratracheal injection of glucose, glucose oxidase, and lactoperoxidase and the other involving the intravenous injection of cobra venom factor (CVF), we investigated the effects of delaying antioxidant administration on the outcome of the inflammatory response. In both cases, the protective effects of catalase and SOD were rapidly attenuated when their administration was delayed for a short period of time. For example, intratracheal catalase resulted in 98% protection when given simultaneously with the glucose oxidase and lactoperoxidase, but only 13% protection when the catalase was delayed 4 min. Likewise, in the CVF-induced lung injury model, intravenous catalase resulted in 40% protection when given simultaneously with the CVF, but only 2% protection when the catalase was delayed 20 min, even though the peak of the injury occurred hours after the initiation of the injury. A similar time dependence was seen with SOD. These results indicate that antioxidant therapy is required early in the course of oxygen radical-mediated acute lung injury for effective protection.