Lipoperoxidation process

Finally the lipoperoxidation process can be fully enzymatic and this is carried out by heme-containing cyclooxigenases (prostaglandin-, tromboxan- and prostacyclin-synthases) or ferrous ione-containing lipoxygenases which are oxidized arachidonic acid and another PUFA by means of free radical mechanism [4,5] as can be seen in Figure 2. 

Oxidative stress is now widely believed to be the major mechanism of athero-genesis. Interestingly, it was demonstrated 47 years ago that atheromatous plaques contain abundant lipoperoxides and other lipid peroxidation products (G9). More recently, our understanding of this process was advanced when evidence was provided for significant free radical activity and the lipid oxidative modification hypothesis was presented (P10). A subsequent study provided further evidence that oxidatively modified low-density lipoproteins (LDL) play a major role in the formation of the fatty streak, the earliest visible atherosclerotic lesion, and the subsequent production of the atheroscelrotic plaque (S27). The proposed sequence, which involves arterial endothelial and smooth muscle cells, as well as mono-cytes/macrophages, is as follows (Ql, S25). 

There are three initiation mechanisms for the free radical lipid peroxidation in the living cells. At the first lipoperoxidation in the body can be induced by non-enzymatic mechanism. In this processes different physical factors such as ionizating irradiation or UV radiation as well as action of some chemical toxicants including air pollutants, pesticides and herbicides from food and drinking water may act as a initiating factors. 

The second initiation way for the lipoperoxidation in the organism can be defined as semi-enzymatic or quasi-enzymatic. During this mechanism the O " radicals are generated by enzymes including NAD(P)H-dependent oxidases of mitochondrial and microsomal electron transport chaines, NADPH-dependent oxidase of phagocytes, xanthine oxidase and other flavine oxidases. After the HO formation the oxidation process develops in non-enzymatic way. 

After one-year exposure to low ozone doses, excess ageing of rabbits was observed. Ozone can affect the ageing process due to the dependence of this process on irreversible cross-linking of macromolecules. Lipoperoxidation can also play a role in this process. 

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