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The role of Fe3+ on Fe2+-dependent lipid peroxidation in phospholipid liposomes.

机译:Fe3 +对磷脂脂质体中Fe2 +依赖性脂质过氧化的作用。

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Fe2+-dependent lipid peroxidation in phosphatidylcholine (PC) liposomes, assessed by thiobarbituric acid-reactive substances (TBARS) production, was stimulated in the presence of Fe3+ in a concentration-dependent manner. The rates of nitroblue tetrazolium (NBT) reduction and Fe2+ oxidation (Fe2+ disappearance and Fe3+ formation) were also enhanced by the addition of Fe3+ to the reaction mixture, and there is a good linear relationship between these parameters. These results suggest that the facilitation of reactive oxygen species (ROS) production via Fe2+ oxidation is closely related to the onset of the stimulatory effect of Fe3+ on Fe2+-dependent lipid peroxidation. On the other hand, results using the liposomes containing various concentrations of endogenous lipid hydroperoxides (LOOH) indicated that endogenous LOOH is not directly involved in the onset of the Fe3+ stimulatory effect on Fe2+-dependent TBARS production and ROS production. This hypothesis was further confirmed by the evidence that Fe2+-dependent ROS production and Fe2+ oxidation of dipalmitoylphosphatidylcholine liposomes were also stimulated by the addition of Fe3+. The results with several antioxidants and radical scavengers suggested that ROS related to Fe2+-dependent lipid peroxidation and its stimulation by Fe3+ are ferrous-oxygen complexes rather than superoxide anion, hydrogen peroxide and hydroxyl radicals. Based on these results, we proposed a possible mechanism for the onset of the Fe3+ stimulation in Fe2+-dependent lipid peroxidation.
机译:在Fe3 +存在下,以浓度依赖的方式刺激磷脂酰胆碱(PC)脂质体中Fe2 +依赖的脂质过氧化作用,通过硫代巴比妥酸反应性物质(TBARS)的产生来评估。通过向反应混合物中添加Fe3 +,也可以提高硝基蓝四唑(NBT)还原和Fe2 +氧化的速率(Fe2 +的消失和Fe3 +的形成),并且这些参数之间具有良好的线性关系。这些结果表明,通过Fe 2+氧化促进活性氧(ROS)的产生与Fe 3+对Fe 2+依赖性脂质过氧化的刺激作用的发生密切相关。另一方面,使用含有各种浓度的内源性脂质氢过氧化物(LOOH)的脂质体的结果表明,内源性LOOH并不直接参与Fe3 +对Fe2 +依赖性TBARS产生和ROS产生的刺激作用的发生。通过添加Fe3 +还可刺激Fe2 +依赖性ROS生成和二棕榈酰磷脂酰胆碱脂质体的Fe2 +氧化,这一假设进一步证实了这一假设。几种抗氧化剂和自由基清除剂的结果表明,与Fe2 +依赖性脂质过氧化及其受Fe3 +刺激有关的ROS是亚铁-氧配合物,而不是超氧阴离子,过氧化氢和羟​​基自由基。基于这些结果,我们提出了Fe2 +依赖性脂质过氧化中Fe3 +刺激发作的可能机制。

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