Videla L A, Villena M I, Donoso G, de la Fuente J, Lissi E
Biochem Int. 1984 Jun;8(6):821-30.
Red blood cells from Wistar rats were exposed to milimolar concentrations of t-butyl hydroperoxide. Extensive hemoglobin oxidation (methemoglobin formation), t-butyl hydroperoxide cleavage (t-butanol formation) and peroxidation (measured by oxygen consumption and thiobarbituric acid reactive substances) was observed. Significant chemiluminescence was emitted by the system. Hemoglobin oxidation and t-butanol production were independent of oxygen pressure and free radical scavengers, however, luminescence was enhanced as oxygen pressure increased and it was reduced by addition of free radical scavengers. The spectral distribution of the light emitted suggests that the luminescence detected is not due to singlet oxygen dimol emission. The results are in agreement with a lipid peroxidative mechanism initiated by t-butoxy radicals produced in the interaction of hemoglobin and t-butyl hydroperoxide.
将来自Wistar大鼠的红细胞暴露于毫摩尔浓度的叔丁基过氧化氢中。观察到广泛的血红蛋白氧化(高铁血红蛋白形成)、叔丁基过氧化氢裂解(叔丁醇形成)和过氧化反应(通过耗氧量和硫代巴比妥酸反应性物质测量)。该系统发出显著的化学发光。血红蛋白氧化和叔丁醇生成与氧压和自由基清除剂无关,然而,随着氧压增加发光增强,并且通过添加自由基清除剂发光减弱。所发射光的光谱分布表明检测到的发光不是由于单线态氧双分子发射。这些结果与血红蛋白和叔丁基过氧化氢相互作用产生的叔丁氧基引发的脂质过氧化机制一致。