Effects of carbon dioxide/bicarbonate on induction of DNA single‐strand breaks and formation of 8‐nitroguanine, 8‐oxoguanine and base‐propenal mediated by peroxynitrite

Yermilov, Vladimir; Yoshie, Yumiko; Rubio, Julieta; Ohshima, Hiroshi

doi:10.1016/s0014-5793(96)01288-4

Cited by 159 publications

(145 citation statements)

References 31 publications

(2 reference statements)

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“…Strand breakage upon treatment with peroxynitrite has been demonstrated previously in plasmid DNA (Yermilov et al, 1996, Epe et al, 1996, Salgo et al, 1995,Yoshie and Ohshima 1997 and cells (Spencer et al, 1996). As in these earlier studies, peroxynitrite formed from SIN-1 induced strand breaks in pUC 18 DNA in this study (Fig.…”

Section: Discussionsupporting

confidence: 88%

Effect of lycopene and β-carotene on peroxynitrite-mediated cellular modifications

Muzandu

Ishizuka

Sakamoto

et al. 2006

Toxicology and Applied Pharmacology

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Peroxynitrite formed by the reaction of superoxide and nitric oxide is a highly reactive species with a role in various pathological processes such as cancer, chronic inflammation, and cardiovascular and neurological diseases. In the present study, the effect of the carotenoids, lycopene and β-carotene, on peroxynitrite-mediated modifications in plasmid DNA as well as cellular DNA and proteins were investigated. In pUC18 plasmid DNA, these carotenoids strongly inhibited DNA strand breaks caused by peroxynitrite generated from 3-morpholinosydnonimine (SIN-1). SIN-1 was also used to determine effects on DNA damage and protein tyrosine nitration in Chinese hamster lung fibroblasts. SIN-1 dose-dependently increased nitration of proteins in cells above basal levels as determined by western blotting. This nitration was inhibited in the presence of the uric acid as well as lycopene. Physiological concentrations (0.31-10 μM) of lycopene and β-carotene also had protective effects on DNA damage, as measured by the comet assay. Lycopene significantly reduced DNA damage particularly, in the median range of concentrations (2.5 μM).The protective effects of lycopene and β-carotene could be due to their scavenging of reactive oxygen (ROS) and/or nitrogen species (RNS) as they reduce the amount of intracellular ROS/RNS produced following treatment with SIN-1 by as much as 47.5 and 42.4 %, respectively. The results obtained in this study suggest that carotenoids may alleviate some of the deleterious effects of peroxynitrite and possibly other reactive nitrogen species as well in vivo.

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Section: Discussionsupporting

confidence: 88%

Effect of lycopene and β-carotene on peroxynitrite-mediated cellular modifications

Muzandu

Ishizuka

Sakamoto

et al. 2006

Toxicology and Applied Pharmacology

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“…The presence of MDA and base propenals was also established qualitatively by thin-layer chromatography (17). An aliquot of the ultrafiltrate prepared from the in vitro reactions above (5 l) was loaded onto a silica gel IB-F TLC plate, resolved with ethyl acetate:isopropyl alcohol:water (74:17:9) and developed by spraying with 0.6% TBA and heating (20 min, 100°C).…”

Section: Methodsmentioning

confidence: 99%

“…These studies are based on disparate reports that: 1) ␥-radiation produces MDA rather than base propenals as the product of 4Ј-oxidation of deoxyribose that accompanies the 3Ј-phosphoglycolate residue (20); 2) ␥-radiation does not cause formation of M 1 dG in DNA (13) (17). The goal was to define the relationship between M 1 dG formation and the generation of MDA or base propenals by deoxyribose 4Ј-oxidants.…”

Section: Correlation Of M 1 Dg Formation With Oxidant-induced Generatmentioning

confidence: 99%

Chemical and Biological Evidence for Base Propenals as the Major Sourceof the Endogenous M1dG Adduct in CellularDNA

Zhou

Taghizadeh

Dedon

2005

Journal of Biological Chemistry

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The endogenous DNA adduct, M 1 dG, has been shown to arise in vitro in reactions of dG with malondialdehyde (MDA), a product of both lipid peroxidation and 4-oxidation of deoxyribose in DNA, and with base propenals also derived from deoxyribose 4-oxidation. We now report the results of cellular studies consistent with base propenals, and not MDA, as the major source of M 1 dG under biological conditions. As a foundation for cellular studies, M 1 dG, base propenals, and MDA were quantified in purified DNA treated with oxidizing agents known to produce deoxyribose 4-oxidation. The results revealed a consistent pattern; Fe 2؉ -EDTA and ␥-radiation generated MDA but not base propenals or M 1 dG, whereas bleomycin and peroxynitrite (ONOO ؊ ) both produced M 1 dG as well as base propenals with no detectable MDA. These observations were then assessed in Escherichia coli with controlled membrane levels of polyunsaturated fatty acids (PUFA). ONOO ؊ treatment (2 mM) of cells containing no PUFA (defined medium with 18:0/stearic acid) produced 6.5 M 1 dG/10 7 deoxynucleotides and no detectable lipid peroxidation products, including MDA, as compared with 3.8 M 1 dG/ 10 7 deoxynucleotides and 0.07 g/ml lipid peroxidation products with control cells grown in a mixture of fatty acids (0.5% PUFA) mimicking Luria-Bertani medium. In cells grown with linoleic acid (18:2), the level of PUFA rose to 54% and the level of MDA rose to 0.14 g/ml, whereas M 1 dG fell to 1.4/10 7 deoxynucleotides. Parallel studies with ␥-radiation revealed levels of MDA similar to those produced by ONOO ؊ but no detectable M 1 dG. These results are consistent with base propenals as the major source of M 1 dG in this model cell system.

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“…Peroxynitrite is ultimately converted to hydroxyl radical and nitrogen dioxide. These free radicals cause tissue damage by the nitration of DNA and proteins, as well as the oxidization of lipids, DNA, and proteins (Beckman, 1996;Yermilov et al, 1996). In addition, NO may produce neuronal death by activating poly (ADP-ribose) synthetase, thereby depleting beta-nicotinamide adenine dinucleotide (Zhang et al, 1994), and inhibiting mitochondrial ATP synthesis as an electron acceptor (Brookes et al, 1999).…”

Section: Production Of Reactive Oxygen Species In Mitochondriamentioning

confidence: 99%

Cellular and Molecular Pathways of Ischemic Neuronal Death

Won¹,

Kim²,

Gwag³

2002

BMB Reports

201

172

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Three routes have been identified triggering neuronal death under physiological and pathological conditions. Excess activation of ionotropic glutamate receptors cause influx and accumulation of Ca 2+ and Na + that result in rapid swelling and subsequent neuronal death within a few hours. The second route is caused by oxidative stress due to accumulation of reactive oxygen and nitrogen species. Apoptosis or programmed cell death that often occurs during developmental process has been coined as additional route to pathological neuronal death in the mature nervous system. Evidence is being accumulated that excitotoxicity, oxidative stress, and apoptosis propagate through distinctive and mutually exclusive signal transduction pathway and contribute to neuronal loss following hypoxic-ischemic brain injury. Thus, the therapeutic intervention of hypoxic-ischemic neuronal injury should be aimed to prevent excitotoxicity, oxidative stress, and apoptosis in a concerted way.

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Effects of carbon dioxide/bicarbonate on induction of DNA single‐strand breaks and formation of 8‐nitroguanine, 8‐oxoguanine and base‐propenal mediated by peroxynitrite

Cited by 159 publications

References 31 publications

Effect of lycopene and β-carotene on peroxynitrite-mediated cellular modifications

Effect of lycopene and β-carotene on peroxynitrite-mediated cellular modifications

Chemical and Biological Evidence for Base Propenals as the Major Sourceof the Endogenous M1dG Adduct in CellularDNA

Cellular and Molecular Pathways of Ischemic Neuronal Death

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