Tang L, Zhang Y, Qian Z, Shen X
Institute of Biophysics, Chinese Academy of Sciences, Datun Road 15, Chaoyang District, Beijing 100101, People's Republic of China.
Biochem J. 2000 Nov 15;352 Pt 1(Pt 1):27-36.
The mechanism of Fe(2+)-initiated lipid peroxidation in a liposomal system was studied. It was found that a second addition of ferrous ions within the latent period lengthened the time lag before lipid peroxidation started. The apparent time lag depended on the total dose of Fe(2+) whenever the second dose of Fe(2+) was added, which indicates that Fe(2+) has a dual function: to initiate lipid peroxidation on one hand and suppress the species responsible for the initiation of the peroxidation on the other. When the pre-existing lipid peroxides (LOOH) were removed by incorporating triphenylphosphine into liposomes, Fe(2+) could no longer initiate lipid peroxidation and the acceleration of Fe(2+) oxidation by the liposomes disappeared. However, when extra LOOH were introduced into liposomes, both enhancement of the lipid peroxidation and shortening of the latent period were observed. When the scavenger of lipid peroxyl radicals (LOO(.)), N,N'-diphenyl-p-phenylene-diamine, was incorporated into liposomes, neither initiation of the lipid peroxidation nor acceleration of the Fe(2+) oxidation could be detected. The results may suggest that both the pre-existing LOOH and LOO(.) are necessary for the initiation of lipid peroxidation. The latter comes initially from the decomposition of the pre-existing LOOH by Fe(2+) and can be scavenged by its reaction with Fe(2+). Only when Fe(2+) is oxidized to such a degree that LOO(.) is no longer effectively suppressed does lipid peroxidation start. It seems that by taking the reactions of Fe(2+) with LOOH and LOO(.) into account, the basic chemistry in lipid peroxidation can explain fairly well the controversial phenomena observed in Fe(2+)-initiated lipid peroxidation, such as the existence of a latent period, the critical ratio of Fe(2+) to lipid and the required oxidation of Fe(2+).
研究了脂质体系统中Fe(2+)引发脂质过氧化的机制。发现在潜伏期内再次添加亚铁离子会延长脂质过氧化开始前的时间滞后。无论何时添加第二剂Fe(2+)，表观时间滞后都取决于Fe(2+)的总剂量，这表明Fe(2+)具有双重功能：一方面引发脂质过氧化，另一方面抑制负责引发过氧化的物质。当通过将三苯基膦掺入脂质体中来去除预先存在的脂质过氧化物(LOOH)时，Fe(2+)不再能引发脂质过氧化，并且脂质体对Fe(2+)氧化的加速作用消失。然而，当向脂质体中引入额外的LOOH时，观察到脂质过氧化增强和潜伏期缩短。当脂质过氧自由基(LOO(·))的清除剂N,N'-二苯基对苯二胺掺入脂质体中时，既检测不到脂质过氧化的引发，也检测不到Fe(2+)氧化的加速。结果可能表明预先存在的LOOH和LOO(·)对于脂质过氧化的引发都是必需的。后者最初来自预先存在的LOOH被Fe(2+)分解，并且可以通过与Fe(2+)反应而被清除。只有当Fe(2+)被氧化到不再有效抑制LOO(·)的程度时，脂质过氧化才开始。似乎通过考虑Fe(2+)与LOOH和LOO(·)的反应，脂质过氧化中的基本化学可以很好地解释在Fe(2+)引发的脂质过氧化中观察到的有争议的现象，如潜伏期的存在、Fe(2+)与脂质的临界比例以及Fe(2+)所需的氧化。
