ascorbic-acid and 1-2-oleoylphosphatidylcholine

Effects of 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC) and moisture on the solubility of hydrophilic and lipophilic antioxidants were evaluated in medium-chain triacylglycerol (MCT) by 2,2-diphenyl-1-picrylhydrazyl (DPPH) reactivity. Next, we assessed the oxidative stability of antioxidant-containing corn oil depending on the presence of DOPC. The critical micelle concentration (CMC) of DOPC decreased when the moisture content was increased from 300 to 495 mg/kg oil and gradually increased when the moisture was further increased to 2122 mg/kg oil. As the DOPC concentration increased, the DPPH reactivity of ascorbyl palmitate in the control MCT increased by 10.23-fold, whereas that of the ascorbic acid and α-tocopherol was slightly affected both by the DOPC and moisture content. Presence of DOPC significantly increased the oxidative stability of ascorbyl palmitate-containing corn oil (p < 0.05), whereas these synergistic antioxidant effects were not observed in ascorbic acid-or α-tocopherol-containing corn oil. In conclusion, DOPC displays a synergistic antioxidant effect with ascorbyl palmitate in bulk oil.

Topics: Antioxidants; Ascorbic Acid; Hydrophobic and Hydrophilic Interactions; Micelles; Oils; Oxidation-Reduction; Phosphatidylcholines; Solubility; Triglycerides

In this contribution an electrochemical study is described for the first time of lipid peroxidation and the role of antioxidant on lipid protection using large unilamellar vesicles (LUVs). In order to simulate the cell membrane, LUVs composed of 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC) were used. A vesicle-modified electrode was constructed by immobilizing DOPC LUVs onto carbon paste electrodes (CPEs). Lipid peroxidation was studied electrochemically by incubating the vesicle-modified electrodes with hydroxyl (HO) radicals generated via the Fenton reaction. Oxidative damage induced by HO was verified by using square wave voltammetry (SWV) and was indirectly measured by the increase of electrochemical peak current to [Fe(CN)

Topics: Antioxidants; Ascorbic Acid; Electrochemical Techniques; Electrodes; Hydrogen Peroxide; Hydroxyl Radical; Iron; Lipid Peroxidation; Phosphatidylcholines; Unilamellar Liposomes

Antioxidant reactions of mixtures of vitamin E, vitamin C and phospholipids in autoxidizing lipids at 90 degrees C have been studied by ESR spectroscopy. When the phospholipid contained a tertiary amine (e.g. phosphatidylcholine), the vitamin C and the vitamin E radicals were successively observed as these two vitamins were sequentially oxidised during lipid oxidation. In the presence of the primary amine contained in phosphatidylserine, the vitamin E oxidation was delayed for a few hours. In this case neither the vitamin C, nor the vitamin E radicals but a nitroxide radical derived from the phospholipid was observed. Similar results to those obtained with PS were obtained in the presence of either phosphatidylethanolamine or soybean lecithin. The participation in the radical reactions of phospholipids possessing a primary amine can therefore explain the synergistic effect of these phospholipids in a mixture of vitamins E and C.

Topics: Ascorbic Acid; Electron Spin Resonance Spectroscopy; Fatty Acids, Unsaturated; Free Radicals; Hot Temperature; Oxidation-Reduction; Phosphatidylcholines; Phosphatidylethanolamines; Phosphatidylinositols; Phosphatidylserines; Phospholipids; Vitamin E

Vitamin E (alpha-tocopherol) is the major lipid-soluble chain-breaking antioxidant of membranes. Its UV-absorbance spectrum (lambda max 295 nm) extends well into the solar spectrum. We hypothesize that in skin alpha-tocopherol may absorb solar UV light and generate tocopheroxyl radicals. Reduction of tocopheroxyl radicals by other antioxidants (e.g. ascorbate, thiols) will regenerate (recycle) vitamin E at the expense of their own depletion. Hence, vitamin E in skin may act in two conflicting manners upon solar illumination: in addition to its antioxidant function as a peroxyl radical scavenger, it may act as an endogenous photosensitizer, enhancing light-induced oxidative damage. To test this hypothesis, we have illuminated various systems (methanol-buffer dispersions, liposomes and skin homogenates) containing alpha-tocopherol or its homologue with a shorter 6-carbon side chain, chromanol-alpha-C6 with UV light closely matching solar UV light, in the presence or absence of endogenous or exogenous reductants. We found that: (i) alpha-tocopheroxyl (chromanoxyl) radicals are directly generated by solar UV light in model systems (methanol-water dispersions, liposomes) and in skin homogenates; (ii) reducing antioxidants (ascorbate, ascorbate+dihydrolipoic acid) can donate electrons to alpha-tocopheroxyl (chromanoxyl) radicals providing for vitamin E (chromanol-alpha-C6) recycling; (iii) recycling of UV-induced alpha-tocopheroxyl radicals depletes endogenous antioxidant pools (accelerates ascorbate oxidation); (iv) beta-carotene, a non-reducing antioxidant, is not active in alpha-tocopherol recycling, and its UV-dependent depletion is unaffected by vitamin E.

Topics: Animals; Antioxidants; Ascorbic Acid; beta Carotene; Carotenoids; Electron Spin Resonance Spectroscopy; Free Radicals; Liposomes; Methanol; Mice; Mice, Hairless; Models, Biological; Neoplasms, Radiation-Induced; Oxygen; Phosphatidylcholines; Radiation Tolerance; Skin; Skin Neoplasms; Suspensions; Thioctic Acid; Ultraviolet Rays; Vitamin E; Water

Dioleoyl phosphatidylcholine (PC) liposomes were ozonized and the ozonized liposomes were tested for their lytic potency on human red blood cells (RBC). Ozonation of PC liposomes generated approximately 1 mole equivalent of hydrogen peroxide (H2O2) and 2 mole equivalents of aldehydes, based on the moles of ozone consumed. The time necessary for 50% hemolysis induced by ozonized liposomes (a convenient measure of hemolytic activity) was found to depend on the extent of ozonation of the PC liposomes, indicating the formation and accumulation of hemolytic agents during ozonation. Hemolysis was also observed when RBC were incubated with nonanal, the expected product of the ozonation of oleic acid, the principle unsaturated fatty acid in the liposomes. Hydrogen peroxide, another product of PC ozonation, did not induce hemolysis; however, a combination of H2O2 and nonanal was significantly more hemolytic than nonanal alone. A ratio of 1:2 H2O2/nonanal (the ratio observed in the ozonized liposomes) provided hemolytic activity comparable to that observed with ozonized dioleoyl PC. Among different antioxidants tested, ascorbate, catalase, and glutathione peroxidase partially inhibited hemolysis induced by ozonized liposomes and by H2O2/nonanal mixtures, but they were not protective against the nonanal-induced hemolysis. Identification of H2O2 and aldehydes as cytotoxic chemical species generated from the ozonation of unsaturated fatty acids may have an important bearing on the in vivo toxicity of ozone on the lung as well as on extrapulmonary tissues.

Topics: Aldehydes; Antioxidants; Ascorbic Acid; Catalase; Erythrocyte Membrane; Hemolysis; Humans; Hydrogen Peroxide; In Vitro Techniques; Lipid Peroxides; Liposomes; Ozone; Phosphatidylcholines; Vitamin E