Membrane lipids peroxidation

Kanner, J. and Harel, S. (1985). Initiation of membranal lipid peroxidation by activated metmyoglobin and methemoglobin. Arch. Biochem. Biophys. 237, 314-321. 

Radi, R., Beckman, J.S., Bush, K.M., and Freeman, B.A. 1991. Peroxynitrite-induced membrane lipid peroxidation The cytotoxic potential of superoxide and nitric oxide. Arch. Biochem. Biophys., 288 481-7. 

Observations Table 2 shows the levels of free radicals determined by luminol chemiluminescence, H202 levels, and membrane lipid peroxidation determined by conjugated dienes. Total free radicals significantly increased by 1.4 fold, hydrogen peroxide significantly decreased 1.3 fold, and lipid peroxidation increased significantly 1.5 fold. 

Maiorino M, Roveri A, Ursini F and Gregolin C. 1985. Enzymatic determination of membrane lipid peroxidation. J Free Radic Biol Med l(3) 203-207. 

Membrane Lipid Peroxidation and Free Radical Formation... 

As discussed above, ufa, which are present primarily in cellular membranes, appear to be particularly susceptible to oxidative degradation by ozone. Various studies of membrane lipid peroxidation have implicated this process in damage to organelles, including mitochondria, micro-somes, and lysosomes, as well as to the cell membrane itself. By analogy, it is conceivable that many of the findings in cells and subcellular components described in other sections of this chapter are secondary to ozone-induced lipid peroxidation. However, this remains conjectural. 

Furthermore, the effects of ozone on the cell membrane do not appear to be limited to ufa. Protein is also affected, particularly cell-membrane sulfhydryl groups and aromatic amino acids. Whether these protein effects are secondaiy to cell-membrane lipid peroxidation or arise as a direct result of ozone is not clear. 

Mechanism of Action A topical agent that binds DNA, inhibiting synthesis of nucleic protein, and reduces mitotic activity. Therapeutic Effect Results in damage to DNA sugar and enhances membrane lipid peroxidation, which may play a critical role in the antipsoriatic action. 

The structural integrity of the cell membrane is irreversibly damaged by the process of membrane lipid peroxidation. The damaged membrane becomes leaky and extracellular calcium enters the cell. This in turn activates calcium-dependent phospholipases and protein kinases, subsequently leading to fatty acid cleavage and other biochemical alterations within the cell. Ultimately this leads to damage or death of the cell. 

Bowman ZS, Morrow JD, JoIIow, DJ, et al. Primaquine induced hemolytic anaemia role of membrane lipid peroxidation and cytoskeletal protein alterations in the hemotoxicity of 5-hydroxyprimaquine. J Pharmacol Exp Ther 2005 314 838-845. 

Lu C., Chan S. L., Haughey N., Lee W. T., and Mattson M. P. (2001). Selective and biphasic effect of the membrane lipid peroxidation product 4-hydroxy-2,3-nonenal on V-methyl-D-aspartate channels. J. Neurochem. 78 577-589. 

Inhibition of biological membrane lipid peroxidation evaluated 366... 

Prevented membrane lipid peroxidation and stopped peroxidation induced by ascorbate, ATP, and Fe3 + in combination (rat) 613... 

Body iron level and iron depletion play an important role in the gender differences seen in death from cardiac disease. There is a better correlation with heart disease mortality in iron levels compared with levels of cholesterol (5). It was found that risk of coronary heart disease (6) and carotid atherosclerosis (7) is associated with increased iron stores. However, impaired endothelium-derived nitric oxide activity may be without overt atherosclerosis in patients with risk factors and may be associated with the presence of atherosclerosis (4). Thus, endothelial dysfunction related to iron activity not only may be an early marker for cardiovascular risk but also may contribute to the pathogenesis of atherosclerosis (2) by the stimulation of low-density lipoproteins (LDL) and membrane lipid peroxidation (I) and may be a key to the understanding of early mechanism in the development of atheroma (7,8). Nakayama et al. (9) showed the role of heme oxygenase induction in the modulation of macrophage activation in atherosclerosis. However, Howes et al. (10) concludes that at the moment, the available evidence on iron hypothesis remains circumstantial. Moreover, Kiechl et al. (7) showed that the adverse effect of iron is hypercholesterolemia, In patients... 

Sevanian, A., Muakkassah-Kelly, S. F., and Montestruque, S. (1983). The influence of phospholipase A2 and glutathione peroxidase on the elimination of membrane lipid peroxides. Arch. Biochem. Biophys. 223, 441-452. 

Perera MI, Katyal SL, Shinozuka H. 1986. Suppression of choline-deficient diet-induced hepatocyte membrane lipid peroxidation in rats by the peroxisome proliferators 4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio(N-beta-hydroxyethyl)acetamide and di(2-ethylhcxyl)phthalate. Cancer Res 46 3304-3308. 

De Vos et al. (1989) suggest that the copper-induced damage to the permeability barrier in roots of Silene cucubalus is caused by a direct metal action on both membrane lipids and thiols. They propose that the first damaging effects of copper ions is the oxidation and cross-linking of membrane protein sulphydryls. However, they also adjudge an important role to the copper induced membrane lipid peroxidation, possibly due to direct free radical formation in the membrane this effect could be enhanced by a depletion of thiols such as glutathione which results in a concomitant decrease of the cellular defence system against free radicals. 

The UV iradiation has been shown to be involved in membrane lipid peroxidation and this induces matrix metalloproteinase-l-expression.38 Therefore, the use of antioxidants has been suggested in treating and preventing skin aging.39 Whether this also works in preventing dry skin in aging is unknown. 

Tsuzuki, T., Igarashi, M., and Miyazawa, T., Conjugated eicosapentaenoic acid (EPA) inhibits transplanted tumor growth via membrane lipid peroxidation in nude mice, J. Nutr., 134, 1162, 2004. 

Coincident with the reduction in brain level of hydroxyl radicals, U-74006F administered at 5 minutes post-injury also acts to reduce post-traumatic opening of the blood-brain barrier (i.e. decreased brain uptake of 14C-albumin) [56]. This effect of U-74006F to close the barrier may be related to the attenuation of hydroxyl-radical levels or an antagonism of the effects of free radicals on the barrier endothelium (i.e. decreased membrane-lipid peroxidation). Indeed, free radicals are known to increase barrier permeability [57]. Consistent with this reduction in post-traumatic opening of the blood-brain barrier which would lead to vasogenic brain edema, U-74006F has been shown to attenuate post-traumatic brain edema in a rat model of fluid percussion head injury [58]. 

OH scavengers such as mannitol and glucose may simply scavenge the extracellular OH without inhibiting lipid peroxidation. Conversely, lipid-soluble OH scavengers such as dimethylthiourea, and antioxidants such as butylated hydroxytoluene (BHT) should effectively inhibit membrane lipid peroxidation (Fig. 1). 

On the basis of this palladium-mediated three-component coupling reaction, Morimoto and co-workers developed a methodology for the synthesis of two novel modified furanoeremophilane-type sesquiterpenes isolated from Trichilia cuneata, the 13-hydroxy-14-nordehydrocacalohastine 72 and 13-acetoxy-14-nordehydrocacalohastine 73 [75]. These two natural products showed inhibitory activities for membrane lipid peroxidation in mitochon-... 

---