13-hydroperoxylinolenic-acid and 15-hydroperoxy-5-8-11-13-eicosatetraenoic-acid

13-hydroperoxylinolenic-acid has been researched along with 15-hydroperoxy-5-8-11-13-eicosatetraenoic-acid* in 2 studies

Other Studies

2 other study(ies) available for 13-hydroperoxylinolenic-acid and 15-hydroperoxy-5-8-11-13-eicosatetraenoic-acid

ArticleYear
Radical adducts of nitrosobenzene and 2-methyl-2-nitrosopropane with 12,13-epoxylinoleic acid radical, 12,13-epoxylinolenic acid radical and 14,15-epoxyarachidonic acid radical. Identification by h.p.l.c.-e.p.r. and liquid chromatography-thermospray-m.s.
    The Biochemical journal, 1991, Jun-01, Volume: 276 ( Pt 2)

    Linoleic acid-derived radicals, which are formed in the reaction of linoleic acid with soybean lipoxygenase, were trapped with nitrosobenzene and the resulting radical adducts were analysed by h.p.l.c.-e.p.r. and liquid chromatography-thermospray-m.s. Three nitrosobenzene radical adducts (peaks I, II and III) were detected; these gave the following parent ion masses: 402 for peak I, 402 for peak II, and 386 for peak III. The masses of peaks I and II correspond to the linoleic acid radicals with one more oxygen atom [L(O).]. The radicals are probably carbon-centred, because the use of 17O2 did not result in an additional hyperfine splitting. Computer simulation of the peak I radical adduct e.p.r. spectrum also suggested that the radical is carbon-centred. The peak I radical was also detected in the reaction of 13-hydroperoxylinoleic acid with FeSO4. From the above results, peak I is probably the 12,13-epoxylinoleic acid radical. An h.p.l.c.-e.p.r. experiment using [9,10,12,13-2H4]linoleic acid suggested that the 12,13-epoxylinoleic acid radical is a C-9-centred radical. Peak II is possibly an isomer of peak I. Peak III, which was observed in the reaction mixture without soybean lipoxygenase, corresponds to a linoleic acid radical (L.). The 12,13-epoxylinoleic acid radical, 12,13-epoxylinolenic acid radical and 14,15-epoxyarachidonic acid radical were also detected in the reactions of linoleic acid, linolenic acid and arachidonic acid respectively, with soybean lipoxygenase using nitrosobenzene and 2-methyl-2-nitrosopropane as spin-trapping agents.

    Topics: Chromatography, High Pressure Liquid; Chromatography, Liquid; Electron Spin Resonance Spectroscopy; Free Radicals; Leukotrienes; Linoleic Acids; Linolenic Acids; Lipid Peroxides; Mass Spectrometry; Molecular Structure; Nitroso Compounds; Spin Labels; Structure-Activity Relationship

1991
Studies on experimentally induced retinal degeneration. 1. Effect of lipid peroxides on electroretinographic activity in the albino rabbit.
    Experimental eye research, 1982, Volume: 35, Issue:2

    Lipid hydroperoxides (LHP) have been synthesized and purified from linoleic, linolenic, arachidonic and docosahexaenoic acids, using soybean lipoxygenase and oxygen. Intravitreal injections into the eyes of mature, albino rabbits produced an early and then progressive decrease in the amplitude of a-, b- and c-waves of the ERG. Depending upon the amount and activity of the LHP preparation, ERG's were markedly decreased in amplitude (greater than 50%) within 4 days following the injection and by 12 days, the activity from peroxide treated eyes was essentially nonrecordable. In preliminary studies, these effects were less pronounced in adult pigmented rabbits of similar age, however, a younger pigmented rabbit was only slightly less susceptible to damage than the albino animals. In other experiments, peroxidized native phospholipids, malonaldehyde, hydrogen peroxide and sodium iodate were also shown to be cytotoxic, but not all were as toxic as the LHP. In contrast, retinol, vitamin A acetate and retinoic acid had no effect upon ERG activity, nor did the parent fatty-acid compounds or the borate buffer in which they were injected. These studies confirm previous reports where indirect production of lipid peroxides caused retinal degeneration. The present report extends these observations to demonstrate that when the retina and RPE are exposed to a sample of purified LHP, retinal function is altered in an irreversible way. We also demonstrate that a metabolic by-product (malonaldehyde) is likewise cytotoxic. However, the mechanisms by which the parent LHP and/or metabolites might act could be quite different. This new animal model should prove useful in evaluating further the ultrastructural changes which are observed during peroxidative damage of the retina in vivo, as well as in evaluating the therapeutic approaches to these problems of retinal degeneration.

    Topics: Animals; Arachidonic Acids; Diterpenes; Docosahexaenoic Acids; Electroretinography; Leukotrienes; Linolenic Acids; Lipid Peroxides; Rabbits; Retina; Retinal Degeneration; Retinyl Esters; Vitamin A

1982