Peroxidation

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Qinshi Zhao - One of the best experts on this subject based on the ideXlab platform.

  • scavenging of reactive oxygen species and prevention of oxidative neuronal cell damage by a novel gallotannin pistafolia a
    Life Sciences, 2002
    Co-Authors: Xingyu Zhao, Qinshi Zhao
    Abstract:

    Pistafolia A is a novel gallotannin isolated from the leaf extract of Pistacia weinmannifolia. In the present investigation, the ability of Pistafolia A to scavenge reactive oxygen species including hydroxyl radicals and superoxide anion was measured by ESR spin trapping technique. The inhibition effect on iron-induced lipid peroxidaiton in liposomes was studied. The protective effects of Pistafolia A against oxidative neuronal cell damage and apoptosis induced by peroxynitrite were also assessed. The results showed that Pistafolia A could scavenge both hydroxyl radicals and superoxide anion dose-dependently and inhibit lipid Peroxidation effectively. In cerebellar granule cells pretreated with Pistafolia A, peroxynitrite-induced oxidative neuronal damage and apoptosis were prevented markedly. The antioxidant capacity of Pistafolia A was much more potent then that of the water-soluble analog of vitamin E, Trolox. The results suggested that Pistafolia A might be used as an effective natural antioxidant for the prevention and cure of neuronal diseases associated with the production of peroxynitrite and related reactive oxygen species.

Placido Navas - One of the best experts on this subject based on the ideXlab platform.

  • role of cytochrome b5 reductase on the antioxidant function of coenzyme q in the plasma membrane
    Molecular Aspects of Medicine, 1997
    Co-Authors: J M Villalba, Francisco Navarro, Consuelo Gomezdiaz, Antonio Arroyo, Rosario I Bello, Placido Navas
    Abstract:

    Abstract Cytochrome b 5 reductase purified from liver plasma membrane reduces coenzyme Q (CoQ) in reconstituted liposomes in the absence of cytochrome b 5 . Both CoQ and its reductase are responsible for the reduction of the ascorbate free radical at the cell surface. Thus, NADH-CoQ reductase represents a partial reaction of NADH-AFR reductase in the plasma membrane. Cytochrome b 5 reductase maintains CoQ and ascorbate in their reduced state to support antioxidations. Reduced CoQ prevents lipid Peroxidation in liposomes and plasma membranes. Also, oxidized CoQ can prevent lipid Peroxidations in the presence of cytochrome b 5 reductase and NADH. Addition of CoQ to intact cells prevents serum withdrawal-induced lipid Peroxidation and apoptosis. The prevention of apoptosis by CoQ is independent of the bcl-2 protein content in the cell. Antioxidants that act at the plasma membrane as CoQ and ascorbate would represent a first barrier to protect lipids from oxidative stress and subsequent apoptosis. Cytochrome b 5 reductase is then an enzyme leading this function at the plasma membrane. These data support the idea that when the plasma membrane barrier fails, bcl-2 protein would be required to prevent cell death.

S Ribarov - One of the best experts on this subject based on the ideXlab platform.

  • lipid Peroxidation in rat lung induced by neuroleptanalgesia and its components
    European Journal of Anaesthesiology, 1998
    Co-Authors: S Chinev, R Bakalova, Sabina Kovacheva, S Ribarov
    Abstract:

    : The aim of the present work was to determine the likelihood of lipid Peroxidation in the lungs of rats subjected to neuroleptanalgesia and its components. In particular, the effect of fentanyl, droperidol, a nitrous oxide/oxygen mixture when used separately or in combination, on the lung level of lipid Peroxidation was investigated. The in vitro antioxidant properties of fentanyl and droperidol were also tested. Lipid Peroxidation was evidenced by the endogenously generated conjugated dienes and fluorescent products of lipid Peroxidation and the decrease in lung vitamin E content. It was found that fentanyl and droperidol, used separately or in combination, did not induce lipid Peroxidation in the rat lung, while the exposure of rats for 120 min to a nitrous oxide/oxygen mixture (2:1 v/v) led to well-expressed Peroxidation. The (N2O + O2)-pro-oxidant action was significantly inhibited in rats previously injected with fentanyl and/or droperidol. The results show that the application of fentanyl, droperidol and (N2O + O2), as in neuroleptanalgesia, ensures minimal lipid Peroxidation in the lung. In addition, we found that fentanyl and droperidol were able to inhibit the Fe(2+)-catalysed lipid Peroxidation in lung homogenate. We speculate that the inhibitory effect of fentanyl and/or droperidol on the (N2O + O2)-induced lipid Peroxidation in the rat lung may be caused directly by their antioxidant properties. However, another explanation seems to be possible. The free radicals that are produced during the metabolism of fentanyl and droperidol may react with the radicals generated during the one-electron reduction of nitrous oxide. Such reactions will obviously reduce the free radical concentration in the organism and, hence, the likelihood of initiating lipid Peroxidation.

Angel Catalá - One of the best experts on this subject based on the ideXlab platform.

  • Non-enzymatic and enzymatic lipid Peroxidation of microsomes and nuclei obtained from rat liver
    Molecular and Cellular Biochemistry, 2004
    Co-Authors: Mónica Marmunti, Mariana Gavazza, Angel Catalá
    Abstract:

    The present study investigates in a experimental system in vitro the relationship between the non-enzymatic (ascorbate-Fe^2+) and enzymatic (NADPH) lipid Peroxidation in rat liver microsomes and nuclei. Chemiluminescence was measured as cpm/mg protein during 180 min at 37 °C. Approximately 50–55% of the fatty acids located in rat liver microsomes and nuclei are polyunsaturated with a prevalence of C18:2 n6 and C20:4 n6. The values of total light emission during the non-enzymatic and enzymatic lipid Peroxidation were highest in microsomes than in nuclei. A significant decrease of C20:4 n6 and C22:6 n3 in rat liver microsomes and nuclei was observed during the lipid ascorbate-Fe^2+-dependent Peroxidation, whereas a significant decrease of C20:4 n6 in rat liver microsomes was observed during enzymatic lipid Peroxidation. Over the time course studies, analysis of chemiluminescence in microsomes and nuclei demonstrated that the lipid Peroxidation in the presence of ascorbate-Fe^2+ reach a maximum at 50 and 30 min, respectively, whereas in the presence of NADPH it reachs a maximum at 20 min in both organelles. In liver microsomes and nuclei the peroxidizability index (pi) which indicates the degree of vulnerability to degradation of a selected membrane showed statistically significant differences between control versus ascorbate-Fe^2+ when microsomes or nuclei were compared. Our results indicate that non-enzymatic (ascorbate-Fe^2+) and enzymatic (NADPH) lipid Peroxidation are operative in rat liver microsomes and nuclei but the sensitivities of both organelles to lipid Peroxidation evidenced by chemiluminescence was greater in the presence of ascorbate-Fe^2+ when compared with NADPH. (Mol Cell Biochem 265: 1–9, 2004)

Xingyu Zhao - One of the best experts on this subject based on the ideXlab platform.

  • scavenging of reactive oxygen species and prevention of oxidative neuronal cell damage by a novel gallotannin pistafolia a
    Life Sciences, 2002
    Co-Authors: Xingyu Zhao, Qinshi Zhao
    Abstract:

    Pistafolia A is a novel gallotannin isolated from the leaf extract of Pistacia weinmannifolia. In the present investigation, the ability of Pistafolia A to scavenge reactive oxygen species including hydroxyl radicals and superoxide anion was measured by ESR spin trapping technique. The inhibition effect on iron-induced lipid peroxidaiton in liposomes was studied. The protective effects of Pistafolia A against oxidative neuronal cell damage and apoptosis induced by peroxynitrite were also assessed. The results showed that Pistafolia A could scavenge both hydroxyl radicals and superoxide anion dose-dependently and inhibit lipid Peroxidation effectively. In cerebellar granule cells pretreated with Pistafolia A, peroxynitrite-induced oxidative neuronal damage and apoptosis were prevented markedly. The antioxidant capacity of Pistafolia A was much more potent then that of the water-soluble analog of vitamin E, Trolox. The results suggested that Pistafolia A might be used as an effective natural antioxidant for the prevention and cure of neuronal diseases associated with the production of peroxynitrite and related reactive oxygen species.