linoleic-acid and phenoxy-radical

We investigated the ability of plasma membrane CoQ reductase (PMQR) purified from pig liver to reduce phenoxyl radicals of a vitamin E homologue, Trolox. We report that NADH-driven one-electron reduction of CoQ0 catalyzed by PMQR produced CoQ0 semiquinone radical and CoQoH2. These in turn, recycle vitamin E homologue, Trolox, via reducing its phenoxyl radical. A significant part of NADH/PMQR-catalyzed reduction of CoQ0 (and Trolox recycling) was superoxide-dependent. Overall, our results demonstrate that PMQR in the model system used can act as an antioxidant enzyme that recycles water-soluble homologues of coenzyme Q and vitamin E.

Topics: Animals; Benzoquinones; Catalysis; Cell Membrane; Chromans; Electron Transport Complex I; Linoleic Acid; Lipoxygenase; NADH, NADPH Oxidoreductases; Oxidation-Reduction; Phenols; Superoxides; Swine; Vitamin E

Free radical reactions of curumin, a lipid soluble antioxidant from turmeric (Curcuma longa), have been studied with a variety of oxidants using TX 100 micelle as a model membrane. The phenoxyl radicals of curcumin generated by one electron oxidizing azide radicals in acetonitrile-water mixture and TX 100 micelles show very similar spectral behavior. However, in membrane models the radical lifetimes and the molar extinction coefficients are significantly different from the homogeneous solutions. Micellized curcumin reacts with haloperoxyl radicals, superoxide, and lipid peroxyl radicals with rate constants of 5 X 10(3), 4.6 X 10(4), and 5.3 X 10(5) M-1s-1, respectively. Curcumin derived phenoxyl radicals decay by radical-radical reactions in homogeneous solutions, while in the micelles, radical decay is mostly first order when the average occupancy of the micelle is less than 1. Implications of these results in evaluating curcumin as an antioxidant is discussed.

Topics: Azides; Curcumin; Free Radicals; Hydrocarbons, Halogenated; Kinetics; Linoleic Acid; Membranes, Artificial; Micelles; Models, Biological; Octoxynol; Phenols; Superoxides

Chain-breaking antioxidants such as butylated hydroxytoluene, alpha-tocopherol, and probucol have been shown to decrease markedly the oxidative modification of low density lipoprotein (LDL). Their mechanism of action appears to involve scavenging of LDL-lipid peroxyl radicals. The purpose of this study was to investigate the occurrence of radical reactions produced during oxidation of LDL and LDL-containing probucol initiated by lipoxygenase or copper. In addition, we have investigated the possibility of a synergistic interaction between ascorbate and probucol in inhibiting the oxidation of LDL. Incubation of LDL-containing probucol and lipoxygenase produced a composite electron spin resonance (ESR) spectrum due to the endogenous alpha-tocopheroxyl radical and probucol-derived phenoxyl radical. The spectral assignment was further verified by chemical oxidation of alpha-tocopherol and probucol. In the presence of ascorbic acid, these radicals in the LDL particle were reduced to their parent compounds with concomitant formation of the ascorbate radical. In both the peroxidation of linoleic acid and the copper-initiated peroxidation of LDL, the antioxidant activity of probucol was significantly increased by low (3-6 microM) concentrations of ascorbate. The probucol-dependent inhibition of LDL oxidation was enhanced in the presence of ascorbic acid. We conclude that the reaction between the phenoxyl radical of probucol and ascorbate results in a synergistic enhancement of the antioxidant capacity of these two compounds and speculate that such reactions could play a role in maintaining the antioxidant status of LDL during oxidative stress in vivo.

Topics: Analysis of Variance; Antioxidants; Ascorbic Acid; Copper; Drug Synergism; Electron Spin Resonance Spectroscopy; Free Radicals; Humans; Linoleic Acid; Linoleic Acids; Lipoproteins, LDL; Oxidation-Reduction; Peroxides; Phenols; Probucol

The 21-aminosteroids U74006F and U74500A have been examined for their ability to scavenge the lipid peroxyl (LOO.) and phenoxy (PhO.) radicals. Lipid peroxidation was followed by measuring the formation of linoleic acid hydroperoxide (LOOH; 18:200H) from linoleic acid during incubations in methanol at 37 degrees C. Initiation of lipid peroxidation was by the radical generator 2,2'-azobis(2,4-dimethylvaleronitrile; AMVN), which under the conditions employed, initiated LOOH formation at a constant rate of 22 microM/h with a kinetic chain length of 21. Alpha-tocopherol (alpha TC) nearly completely blocked the chain reaction by scavenging LOO., reducing its formation to that essentially attributable to initiation alone. The average inhibition rate constant kinh for alpha TC at 37 degrees C was calculated as 4.9 x 10(5) M-1 sec-1. U74006F or U74500A also inhibited LOOH formation, reducing its rate to a constant fraction of control in a concentration dependent manner. U74500A was a more potent scavenger of LOO. than U74006F; however, both compounds were considerably less potent than alpha TC based upon their respective kinh's at 37 degrees C. Similarly, alpha TC, U74006F and U74500A scavenged PhO.. As seen with LOO. scavenging, alpha TC was orders of magnitude more reactive toward PhO. than either 21-aminosteroid as judged by their respective second order rate constants (k2). Both U74006F and U74500A were degraded during their reaction with LOO. or PhO. to as yet uncharacterized product(s). The data indicate that while the 21-aminosteroids can scavenge lipid radicals, their activity in this regard is less than expected based upon their ability to inhibit iron dependent lipid peroxidation.

Topics: Antioxidants; Kinetics; Linoleic Acid; Linoleic Acids; Lipid Peroxidation; Lipid Peroxides; Peroxides; Phenols; Pregnatrienes