Panasenko O M, Arnhold J, Arnhold K, Vladimirov Iu A, Sergienko V I
Institute of Medical Physics and Biophysics, University Leipzig, Germany.
Biofizika. 1996 Mar-Apr;41(2):334-41.
The present study examined the kinetics of accumulation of lipid peroxidation products in phosphatidylcholine liposomes incubated with hypochlorite (HOCl/OCl-) or with FeSO4 in the presence of ascorbate. The incubation of liposomes with HOCl/OCl- led to the accumulation of primary (lipid hydroperoxides and conjugated dienes) and secondary (TBA-reactive substances) lipid peroxidation products identical to those generated in the presence of Fe2+/ascorbate. However the rate of the formation of lipid peroxidation products as well as the gain in their amount were sufficiently higher (4-150-fold and 3-6-fold, respectively) in the case of HOCl/OCl(-)-induced lipid peroxidation as compared to lipid peroxidation in the Fe2+/ascorbate system. The accumulation of lipid peroxidation products lasted until HOCl/OCl- was present in the reaction mixture. The data obtained support our hypothesis that hypochlorite produced by activated neutrophils and monocyte/macrophages may be reasonable for the initiation of lipid peroxidation in blood.
本研究检测了在次氯酸盐（HOCl/OCl-）存在下或在抗坏血酸盐存在时与硫酸亚铁一起孵育的磷脂酰胆碱脂质体中脂质过氧化产物的积累动力学。脂质体与HOCl/OCl-孵育导致初级（脂质氢过氧化物和共轭二烯）和次级（TBA反应性物质）脂质过氧化产物的积累，这些产物与在Fe2+/抗坏血酸盐存在下产生的产物相同。然而，与Fe2+/抗坏血酸盐体系中的脂质过氧化相比，HOCl/OCl(-)诱导的脂质过氧化情况下脂质过氧化产物的形成速率及其量的增加分别足够高（分别为4-150倍和3-6倍）。脂质过氧化产物的积累一直持续到反应混合物中存在HOCl/OCl-。获得的数据支持我们的假设，即活化的中性粒细胞和单核细胞/巨噬细胞产生的次氯酸盐可能是血液中脂质过氧化起始的原因。
