Liposomes as a Tool to Study Lipid Peroxidation

Abstract

Cell membrane lipids (phospholipids, glycolipids and cholesterol) are the most common substrates of oxidative attack. Once initiated reaction autocatalytic continues, it has progradient flow, and the ultimate consequence is the structural-functional changes of the substrate. Lipid peroxidation is one of the best studied processes of cell damage under conditions of oxidative stress [3-5]. In 1960s Hochstein et al. [6] found that the initiation of lipid peroxidation require the presence of iron ions. From that moment the mechanism of lipid peroxidation process has been studied in many in vitro systems. However, accurate and precise mechanism is still not fully understood. Peroxidation in liposomes is usually studied after adding iron ions (Fe2+ plus ascorbic acid). Although the mechanism is not fully understood, it is known that redox chemistry of iron plays an important role in the occurrence and the rate of lipid peroxidation. Many studies have shown that the irondependent lipid peroxidation in systems comprised initially of Fe2+ and liposomes requires Fe2+ oxidation. In their research work, Minotti and Aust [7] assumed that the complex is formed between Fe2+ and Fe3+ ions could be initiator of iron-dependet lipid peroxidation. However, the existence of this complex has never been proven. In contrast, Aruoma et al. [8] argue against the participation of a Fe2+-Fe3+-O2 complex, or a critical 1:1 ratio of Fe2+ to Fe3+, in the initiation of lipid peroxidation in liposomes. Study of Tang et al. [9] showed that whether adding 100 or 150 mM Fe2+ initially or adding 100 mM Fe2+ initially and then 50 mM Fe2+ later at various times during the latent period in the liposomal system, the concentration of the remaining Fe2+ at the end of the latent period was almost the same every time.