Oxidized phospholipids formation

A second important series of experiments dealt with membrane chemistry composed of 5-cho1esten-3B-o1 (cholesterol) and partially oxidized phospholipid. The ultraviolet radiation Induced oxidation led to formation of hydroperoxide moieties at the unsaturated sites on some of the phospholipid acyl chains listed In Table II. The Cjg 2 chain was chosen as a reactive representative... 

Podrez, E.A. et al. A novel family of atherogenic oxidized phospholipids promotes macrophage foam cell formation via the scavenger receptor CD36 and is enriched in atherosclerotic lesions 1. J. Biol. Chem. 277 (2002a) 38517-23. 

Subbanagounder, G., Wong, J.W., Lee, H., FauU, K.F., Miller, E., Witztum, J.L., and Berhner, J.A. 2002. Epoxyisoprostane and epoxycyclopentenone phospholipids regulate monocyte chemotactic protein-1 and interleukin-8 synthesis. Formation of these oxidized phospholipids in response to interleukin-Ibeta. /. Biol. Chem.. 277, 7271-7281. 

Extensive studies in vitro from many groups have confirmed that exposure of LDL to a variety of pro-oxidant systems, both cell-free and cell-mediated, results in the formation of lipid hydroperoxides and peroxidation products, fragmentation of apoprotein Bioo, hydrolysis of phospholipids, oxidation of cholesterol and cholesterylesters, formation of oxysterols, preceded by consumption of a-tocopherol and accompanied by consumption of 8-carotene, the minor carotenoids and 7-tocopherol. 

Schnurr et al. [22] showed that rabbit 15-LOX oxidized beef heart submitochondrial particles to form phospholipid-bound hydroperoxy- and keto-polyenoic fatty acids and induced the oxidative modification of membrane proteins. It was also found that the total oxygen uptake significantly exceeded the formation of oxygenated polyenoic acids supposedly due to the formation of hydroxyl radicals by the reaction of ubiquinone with lipid 15-LOX-derived hydroperoxides. However, it is impossible to agree with this proposal because it is known for a long time [23] that quinones cannot catalyze the formation of hydroxyl radicals by the Fenton reaction. Oxidation of intracellular unsaturated acids (for example, linoleic and arachidonic acids) by lipoxygenases can be suppressed by fatty acid binding proteins [24]. 

In addition, there is experimental evidence showing that mitochondrial cardiolipin content markedly decreases following ischemia and reperfusion injury due to cardiolipin peroxidation (Soussi et al., 1990) and that a decrease in the mitochondrial phospholipid cardiolipin occurred in aged rat hearts (Pepe, 2000). These decreases may he attrihutahle to the hydroperoxide-formation of cardiolipin after exposure to intense or repeated oxidative stress during disease state or normal aging, respectively. 

Two conditions in which the rate of ketone body formation is increased are hypoglycaemia and prolonged starvation in adults or short-term starvation in children. What is the mechanism for increasing the rate Although there are several fates for fatty acids in the liver, triacylglycerol, phospholipid and cholesterol formation and oxidation via the Krebs cycle, the dominant pathway is ketone body formation (Figure 7.20). Three factor regulate the rate of ketone body formation (i) hormone sensitive lipase activ-... 

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