Barrier L, Page G, Fauconneau B, Juin F, Tallineau C
Laboratoire de Biochimie et Toxicologie, Hôpital Jean Bernard, Poitiers, France.
Free Radic Res. 1998 Apr;28(4):411-22. doi: 10.3109/10715769809070810.
Aerobically-incubated brain homogenates are known to undergo autoxidation characterized by spontaneous TBARS production, presumably as a result of lipid peroxidation. However, TBARS measurement alone, because of its lack of specificity, is not sufficient to demonstrate the occurrence of lipid peroxidation in complex biological systems. This study, undertaken to determine whether or not spontaneous oxidation of rat brain homogenate is due to lipid peroxidation, measured different specific markers of this process (fatty acids, lipid aldehydes and the formation of fluorescence products) and studied changes in alpha-tocopherol. Incubation of rat brain homogenates at 37 degrees C under air led to spontaneous TBARS formation, which was accompanied by lipid aldehydes and lipid fluorescence products as well as polyunsaturated fatty acid (PUFA) degradation. Alpha-tocopherol was also consumed. On the whole, these results demonstrate that autoxidation of brain homogenate is a spontaneous lipid peroxidation process. When homogenates were exposed to Fe2+ and ascorbic acid-induced oxidative stress, lipid peroxidation was enhanced. However, spontaneous and stimulated peroxidation showed similar patterns not characteristic of classical lipid peroxidation, i.e. without the lag and accelerating phases typical of a propagating chain reaction. PUFA degradation was limited despite stimulation of peroxidation.
已知需氧孵育的脑匀浆会发生以自发产生硫代巴比妥酸反应物（TBARS）为特征的自氧化作用，这可能是脂质过氧化的结果。然而，仅测量TBARS，由于其缺乏特异性，不足以证明在复杂生物系统中发生了脂质过氧化。本研究旨在确定大鼠脑匀浆的自发氧化是否归因于脂质过氧化，测量了该过程的不同特异性标志物（脂肪酸、脂质醛和荧光产物的形成）并研究了α-生育酚的变化。在空气中于37℃孵育大鼠脑匀浆会导致自发形成TBARS，同时伴有脂质醛、脂质荧光产物以及多不饱和脂肪酸（PUFA）降解。α-生育酚也会被消耗。总体而言，这些结果表明脑匀浆的自氧化是一个自发的脂质过氧化过程。当匀浆暴露于Fe2+和抗坏血酸诱导的氧化应激时，脂质过氧化会增强。然而，自发和刺激的过氧化表现出类似的模式，并非典型脂质过氧化的特征，即没有典型的传播链反应的滞后和加速阶段。尽管过氧化受到刺激，但PUFA降解受到限制。
