Brain lipid oxidation

Briner, W., Murray, J. (2005). Effects of short-term and long-term depleted uranium exposure on open-field behavior and brain lipid oxidation in rats. Neurotoxicol. Teratol. 27 135 4. 

Parrado, J. Miramontes, E. Jover, M. Marquez, J.C. Angeles Mejias, M. Collantes De Teran, L. Absi, E. Bautista, J. 2003. Prevention of brain protein and lipid oxidation elicited by a water-soluble oryzanol enzymatic extract derived from rice bran. Eur. J. Nutr. 42 307-314. 

Matsmoto K, Yobimoto K, Huong NT, Abdel-Fattah M, Van Hien T, Watanabe H. Psychological stress-induced enhancement of brain lipid peroxidation via nitric oxide systems and its modulation by anxiolytic and anxiogenic drugs in mice. Brain Res 1999 839 74—84. 

Lipid Composition. After the behavior experiments, the rats were killed by decapitation. Tissue samples including brain and retina were removed and stored at -80°C. The total lipid extracts of tissues were prepared according to the method of Folch et al. (39). Butylated hydroxytoluene (300 qg/sample) was added in methanol to each sample to minimize lipid oxidation. The total lipid extracts were trans-methylated with 14% BFj/methanol at 100°C for 60 min by a modification (40) of the method of Morrison and Smith (41). Fatty acid methyl esters were then analyzed on a Hewlett-Packard 5890 gas chromatograph (Hewlett-Packard, Palo Alto, CA) equipped with a flame ionization detector and fused silica capillary column (DB-FFAP, 30 m X 0.25 mm x 0.25 m, J W, Folsom, CA) with carrier gas (hydrogen) at a linear velocity of 50 cm/s. Injector and detector temperature were set to 250°C and oven temperature program was as follows 130 to 175°C at4°C/min, 175 to 210°C at l°C/min, and then to 245 at 30°C/min, with a final... 

The scale of the all changes substantially depends on the values for the initial lipids. So, the formation of liposomes from the murine organ lipids brought out the enhancement of the membrane rigidity (the increase of the PC/PE ratio), the more pronounced under the formation of liposomes from the brain lipids (Table 1), while the diminution of the ability of lipids to the oxidation is obtained in case the EEOPL/ZPOPL ratio is more than 0.7 in lipids of the murine organs (Table 1). 

The incorporation of LA and CLA isomers into cellular phospholipids has different effects on lipid peroxidation measured as oxygen consumption (Fig. 10.8—10.11). PC(SA LA) at a level of 5 mol% of total fatty acids reduced oxygen consumption in all of the tested PC liposome systems (Fig. 10.8—10.11), while 5 mol% PC(SA c9,rl 1-CLA) increased oxygen consumption in liposomes prepared with PC(soy) and PC(egg yolk), but reduced it in PC(rat heart) and PC(rat brain) liposomes. These data indicated that PC(SA cS,tl 1-CLA) may exhibit antioxidant or pro-oxidant properties in different phospholipids systems including membranes. Interestingly, PC(SA rlO,differed from both PC(SA LA) and PC(SA c9,t 1-CLA) in its influence on lipid peroxidation in liposome prepared with different PC. Incorporation of 5 mol% PC(SA rlO,cl2-CLA) decreased lipid oxidation in the soy PC liposomes (Fig. 10.8), but increased lipid oxidation in the liposomes prepared from all the other PC, egg, rat heart, and rat brain (Fig. 10.9—10.11). 

Oxidative stress induced by chronic administration of naphthalene (llOmg/kg rat x day p.o. in corn oil up to 120 days) resulting in tissue damaging effects as maximum increases in hepatic and brain lipid peroxidation and DNA fragmentation was reported by Bagchi et al. (1998). 

Membrane lipids are particularly vulnerable to oxidation due to their high content in polyunsaturated acyl chains. The oxidation of membrane lipids generates important changes in their physicochemical properties, thereby significantly affecting membrane behavior. Two main pathways of oxidation of polyunsaturated acyl chains include enzymatic and nonen-zymatic mechanisms.Membrane cholesterol also provides an oxidation pathway. Oxidation of membrane lipids occurs upon aging and in neurodegenerative diseases. Indeed, postmortem analysis has indicated that the extent of lipid oxidation in brains affected by Alzheimer s disease exceeds that in age-matched control individuals. The main oxidized forms of cholesterol found in brain tissue are listed in Fig. 3.24. 

The main route of energy provision from fatty acids is the 3-oxidation pathway in which carbon atom C-3 (p-carbon) is oxidized. In man, other pathways also exist. The a-oxidation pathway which involves the oxidation of the C-2 atom is important in the degradation of ingested branched fatty acids and brain lipids to prepare such fatty acids for entry into the P-oxidation route. The ca (omega)-pathway involves the oxidation of the terminal methyl group primarily of to C, fatty acids. The dicarboxylate product enters the p-oxidation pathway. 

O Brian CA, Ward NE, Weinstein IB, Bull AW, Marnett LJ. Activation of rat brain protein kinase C by lipid oxidation products. Biochem Biophys Res Commun 1988 155 1374-1380. 

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