Rosen G M, Freeman B A
Proc Natl Acad Sci U S A. 1984 Dec;81(23):7269-73. doi: 10.1073/pnas.81.23.7269.
Superoxide and lipid free-radical generation in cultured endothelial cells treated with menadione or nitrazepam were measured using electron paramagnetic resonance spectroscopy. Superoxide was detected both intracellularly and extracellularly. Extracellular generation of superoxide and hydrogen peroxide was also measured, either by spectrophotometric measurement of succinoylated cytochrome c reduction or by polarography. Extracellular superoxide was generated due to reduced menadione diffusing across the plasma membrane and reacting with oxygen to generate superoxide in the medium. Increased intracellular oxygen tension favored intracellular oxidation of reduced menadione, thus decreasing diffusion of reduced menadione from the cells and, hence, decreasing extracellular superoxide production. The nitro anion free radical of reduced nitrazepam, which cannot cross the plasma membrane, did not generate detectable extracellular superoxide. Our results show that intracellular superoxide can be spin-trapped using 5,5-dimethyl-1-pyrroline-1-oxide and that secondary free-radical injury to membrane lipids, due to excess production of partially reduced species of oxygen by intact cells, can be detected by spin-trapping lipid free radicals with phenyl N-tert-butylnitrone.
利用电子顺磁共振波谱法测定了用甲萘醌或硝西泮处理的培养内皮细胞中超氧化物和脂质自由基的生成情况。在细胞内和细胞外均检测到了超氧化物。还通过分光光度法测定琥珀酰化细胞色素c还原或极谱法来测量超氧化物和过氧化氢的细胞外生成情况。细胞外超氧化物是由于还原型甲萘醌扩散穿过质膜并与氧气反应在培养基中生成超氧化物而产生的。细胞内氧张力增加有利于还原型甲萘醌的细胞内氧化,从而减少还原型甲萘醌从细胞中的扩散,进而减少细胞外超氧化物的产生。还原型硝西泮的硝基阴离子自由基不能穿过质膜,不会产生可检测到的细胞外超氧化物。我们的结果表明,细胞内超氧化物可以用5,5-二甲基-1-吡咯啉-1-氧化物进行自旋捕获,并且完整细胞过量产生部分还原的氧物种导致的对膜脂质的继发性自由基损伤,可以通过用苯基N-叔丁基硝酮自旋捕获脂质自由基来检测。