Kikkawa Y, Yano S, Skoza L
Lab Invest. 1984 Jan;50(1):62-71.
Interferon inducers, poly I:poly C, endotoxin, hepatic RNA, and Tilorone, were administered to rats at different time points in relation to the onset of hyperoxic exposure (O2 greater than 97%). All interferon inducers tested significantly reduced the mortality of rats when compared with the control groups. In hyperoxia alone, malondialdehyde, a product of lipid peroxidation, was significantly increased and the microsomal enzyme NADPH cytochrome c reductase decreased as measured in the whole lung. With the administration of either endotoxin or poly I:poly C these two parameters remained within the range of control values. These data suggest that the administration of interferon inducers protects against hyperoxic microsomal damage. After the administration of these interferon inducers with or without hyperoxia the increased activity of heme oxygenase and marked reduction of the heme content of microsomes were demonstrated. Since cytochrome P-450 and b5 are the major hemoproteins of microsomes and the known source of oxygen-free radical generation, the results obtained in this study appear to indicate that the depression of the hemoprotein of microsomes by the administration of interferon inducers may be largely responsible for the protective effects of these agents against hyperoxia.
在与高氧暴露（氧气浓度大于97%）开始相关的不同时间点，给大鼠施用干扰素诱导剂、聚肌胞苷酸、内毒素、肝RNA和泰洛龙。与对照组相比，所有测试的干扰素诱导剂均显著降低了大鼠的死亡率。仅在高氧环境下，脂质过氧化产物丙二醛显著增加，全肺中微粒体酶NADPH细胞色素c还原酶减少。施用内毒素或聚肌胞苷酸后，这两个参数仍保持在对照值范围内。这些数据表明，施用干扰素诱导剂可预防高氧引起的微粒体损伤。施用这些干扰素诱导剂后，无论有无高氧暴露，均显示血红素加氧酶活性增加，微粒体血红素含量显著降低。由于细胞色素P-450和b5是微粒体的主要血红素蛋白，也是已知的氧自由基产生来源，本研究获得的结果似乎表明，施用干扰素诱导剂导致微粒体血红素蛋白减少可能在很大程度上是这些药物对高氧具有保护作用的原因。
