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Interactions of Nitric Oxide with Lipid Peroxidation Products under Aerobic Conditions: Inhibitory Effects on the Formation of Malondialdehyde and Related Thiobarbituric Acid-Reactive Substances
Affiliation:1. Department of Organic and Biological Chemistry, University of Naples Federico II, Via Mezzocannone 16, I-80134, Naples, Italy;2. Stazione Zoologica, Villa Comunale, 80121, Naples, Italy;1. Division of Urology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan;2. Department of Urology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu 431-3192, Japan;1. Department of Physiology, Basic Medical College, Xinjiang Medical University, Urumqi 830011, China;2. Department of Histology and Embryology, Basic Medical College, Xinjiang Medical University, Urumqi 830011, China;3. Center of Morphology, Basic Medical College, Xinjiang Medical University, Urumqi 830011, China;1. Department of Agronomy, University of Almería, ceiA3, 04120 Almería, Spain;2. Cajamar Research Center “Las Palmerillas”, 04710 El Ejido, Almería, Spain;1. Department of Chemistry and Industrial Chemistry, University of Genoa, Via Dodecaneso 31, I-16146 Genoa, Italy;2. Department of Biosciences, Biotechnologies, and Biopharmaceutics, University of Bari Aldo Moro, via E. Orabona 4, 70126 Bari, Italy;3. Department of Pharmacy – Drug Sciences, University of Bari Aldo Moro, via E. Orabona 4, 70126 Bari, Italy;1. Ariel University, Faculty of Natural Sciences, Physics Department, 407000, P.O.B. 3, Ariel, Israel;2. Ariel University, Chemical Engineering and Biotechnology Department, 40700, P.O.B. 3, Ariel, Israel
Abstract:Under aerobic conditions, exposure of peroxidized lipids to nitric oxide (NO) was found to result in a rapid decrease in the levels of thiobarbituric acid-reactive substances (TBARS). Addition of 10–100 μM NO to rat brain homogenates preincubated for 2 h at 37°C caused up to a 20% decrease in the levels of TBARS compared to controls. A similar inhibitory effect was observed on TBARS produced by Fe2+-induced decomposition of 15-hydroperoxyeicosatetraenoic acid (15-HPETE), due apparently to NO-induced decomposition of the hydroperoxide (ferrous oxidation/xylenol orange assay). Prostaglandin G2 (PGG2, 35 μM), as a model bicyclic endoperoxide, and malondialdehyde (MDA, 20 μM), the main component of TBARS, proved also susceptible to degradation by NO or NO donors (diethylamine NONOate, DEA/NO) at concentrations of 100 μM or higher in 0.05 M phosphate buffer, pH 7.4, and at 37°C, as indicated by the reduced response to the TBA assay. No significant effect on TBARS determination was caused by nitrite ions. These and other data indicate that NO can inhibit TBARS formation by decomposing primary lipid peroxidation products, chiefly 15-HPETE and related hydroperoxides, and, to a lesser extent, later stage TBARS precursors, including bicyclic endoperoxides and MDA, via nitrosation and other oxidative routes, without however affecting chromogenic reactions during the assay.
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