Antioxidant and pro-oxidant actions of flavonoids: effects on DNA damage induced by nitric oxide, peroxynitrite and nitroxyl anion

Ohshima, Hiroshi; Yoshie, Yumiko; Auriol, Sebastien; Gilibert, Isabelle

doi:10.1016/s0891-5849(98)00141-5

Cited by 213 publications

(124 citation statements)

References 38 publications

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“…22,23 The impairment of proteins and DNA by ONOO Ϫ has been studied thoroughly. [15][16][17][18][19] In addition, ONOO Ϫ induces nitration of proteins and DNA. Many investigators have reported that nitration of tyrosine residues impaired the function of the protein by suppressing the phosphorylation of the protein and decreasing the enzyme activity.…”

Section: Discussionmentioning

confidence: 99%

“…28 In these modifications, tyrosine nitration has been extensively explored with the aim of analysis of the cytotoxic mechanism of ONOO Ϫ . [15][16][17]29 A few investigators reported nitration of cytochrome c and s-nitrosylation of caspase 3 by ONOO Ϫ , but they did not examine the influence of nitration on the catalytic and proteolytic activities of these proteins. 30 -32 Cytochrome c and procaspase 3 have 4 and 10 tyrosine residues, respectively.…”

mentioning

confidence: 99%

“…13,14 The reactant ONOO Ϫ vigorously damages cells by impairment of proteins and DNA. [15][16][17][18][19] Inactivation of the proapoptotic proteins by ONOO Ϫ is therefore probable in chemoradiotherapy of cancers although the apoptosis-inducing activity of ONOO Ϫ has been demonstrated in multiple kinds of cancer cells. 20,21 NO reacts with molecular oxygen (O 2 ), O 2 Ϫ and transitional metals, yielding nitrogen dioxide (NO 2 ), ONOO Ϫ and metalnitrosyl adducts, respectively.…”

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confidence: 99%

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Tyrosine‐nitration of caspase 3 and cytochrome c does not suppress apoptosis induction in squamous cell carcinoma cells

Ueta

Kamatani

Yamamoto

et al. 2002

Intl Journal of Cancer

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The influence of tyrosine nitration of cytochrome c and caspase 3 on apoptosis induction was investigated in an established squamous carcinoma cell line, OSC-4. The intracellular NO and O 2 ؊ levels were increased up to about 110 -120% and 140 -180% of the control levels, respectively, after the treatment of OSC-4 cells with 5-FU (100 g/ml), PLM (10 g/ml), CDDP (10 g/ml), or ␥-rays (20 Gy). The treatment of OSC-4 cells with ONOO ؊ (1 mM) and the above anticancer agents induced tyrosine nitration of 14, 32 kDa protein among others and nitration of tyrosine residues of cytochrome c and caspase 3 was identified by the Western blotting of immunoprecipitates obtained by antibodies to these proapoptotic proteins. When cytochrome c and procaspase 3 were treated with ONOO ؊ , tyrosine nitration was increased in a ONOO ؊ -dose dependent manner. Tyrosine nitration of cleaved (17 kDa) Key words: tyrosine-nitration; caspase 3; cytochrome c; apoptosis; squamous cell carcinoma cells; anticancer agentsSuccessful anticancer therapy with chemicals and radiation strongly depends on the strategy for differentiation and apoptosis induction of cancer cells. ROS induce apoptotic signals in cancer cells and apoptosis induction by anticancer drugs and ␥-rays is closely associated with intracellular ROS generation. [1][2][3][4][5][6][7] Apoptotic signals are transduced mainly through 2 pathways, one of which is originates from the mitochondria and the other is the Fas-associated route. 8 -10 The release of the main mitochondrial proapoptotic protein, cytochrome c, is under the regulation of ROS. 11,12 In addition to the generation of ROS, NO is also generated in anticancer drug-and ␥-ray-treated cancer cells and reaction of ROS with NO is allowed in a favorable circumstance. 13,14 The reactant ONOO Ϫ vigorously damages cells by impairment of proteins and DNA. [15][16][17][18][19] Inactivation of the proapoptotic proteins by ONOO Ϫ is therefore probable in chemoradiotherapy of cancers although the apoptosis-inducing activity of ONOO Ϫ has been demonstrated in multiple kinds of cancer cells. 20,21 NO reacts with molecular oxygen (O 2 ), O 2 Ϫ and transitional metals, yielding nitrogen dioxide (NO 2 ), ONOO Ϫ and metalnitrosyl adducts, respectively. 22-24 These reactants are highly reactive and exhibit a variety of physiological activities. 25 In many disorders including inflammatory diseases, the neurotoxicity of stroke, Alzheimer's disease, Parkinson's disease and multiple sclerosis, the highly reactive nitrogen chemicals, especially ONOO Ϫ , are deeply associated with the pathological degeneration of the tissues although the half life of ONOO Ϫ is very short, less than one second in the physiological condition. 26,27 ONOO Ϫ has a potential to cause DNA-strand breaks, lipid peroxidation and diverse modification of cellular molecules such as oxidation of thiol and methionine and nitration of tyrosine and tryptophane. 28 In these modifications, tyrosine nitration has been extensively explored with the aim of analysis of the cytotoxic mec...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Tyrosine‐nitration of caspase 3 and cytochrome c does not suppress apoptosis induction in squamous cell carcinoma cells

Ueta

Kamatani

Yamamoto

et al. 2002

Intl Journal of Cancer

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“…However, when purified DNA was exposed to NO at concentrations as high as 1.0 M, single stand breaks were not observed [86]. Nitric oxide is also reported to protect DNA against oxidative stress by inhibiting Fenton reaction of hydrogen peroxide which leads to single strand generation [87]. It has also been reported that NO in presence of a flavonoid having orthotrihydroxy group namely epigallocatechingallate or quercetogelin inhibits DNA damage by preventing formation of 8-nitroguanine in calf thymus DNA.…”

Section: Anti-tumor Effect Of Nomentioning

confidence: 99%

Biochemistry of Nitric Oxide

2011

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Nitric oxide (NO) a free radical having both cytoprotective as well as tumor promoting agent is formed from L-arginine by converting it to L-citrulline via nitric oxide synthase enzymes. The reaction product of nitric oxide with superoxide generates potent oxidizing agent, peroxynitrite which is the main mediator of tissue and cellular injury. Peroxynitrite is reactive towards many biomolecules which includes amino acids, nucleic acid bases; metal containing compounds, etc. NO metabolites may play a key role in mediating many of the genotoxic/ carcinogenic effects as DNA damage, protein or lipid modification, etc. The basic reactions of nitric oxide can be divided as direct effect of the radical where it alone plays a role in either damaging or protecting the cell milieu and an indirect effect in which the byproducts of nitric oxide formed by convergence of two independent radical generating pathways play the role in biological reactions which mainly involve oxidative and nitrosative stress. Nitric oxide is also capable of directly interacting with mitochondria through inhibition of respiration or by permeability transition. Reaction of nitric oxide with metal ions include its direct interaction with the metals or with oxo complexes thereby reducing them to lower valent state. Excessive production of nitric oxide can be studied by inhibiting the synthetic pathway of nitric oxide using both selective or specific nitric oxide synthase inhibitor or nonselective nitric oxide synthase inhibitor with respect to isoforms of nitric oxide.Keywords Nitric oxide Á Nitric oxide synthase Á Nitric oxide inhibitors Á Generation of nitric oxide Á Cancer Á Systemic lupus erythematosus Á Direct and indirect effect of nitric oxide Á Effect of nitric oxide on mitochondria

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“…They can potentially bind to double stranded DNA (dsDNA). Depending on reaction conditions antioxidative as well as prooxidative activities of flavonoids have been found in various systems [17][18][19][20]. , in the presence of hydrogen peroxide and ascorbic acid was used as the cleavage mixture producing reactive oxygen species (ROS).…”

Section: Introductionmentioning

confidence: 99%

Voltammetric Detection of Antioxidative Properties of Flavonoids Using Electrically Heated DNA Modified Carbon Paste Electrode

Korbut

Bučková

Labuda

et al. 2003

Sensors

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Abstract:A simple electrochemical sensor consisting of electrically heated carbon paste electrode with the surface modified by dsDNA is used to characterize voltammetric behaviour and antioxidative activity of four selected flavonoids. Quercetin, rutin, catechin and epigallocatechin gallate accumulate within the DNA layer. A positive effect of the electrode temperature within the range of 20 to 38 ºC on the detection of a deep DNA degradation by a copper(II)/H 2 O 2 /ascorbic acid cleavage mixture as well as an antioxidative effect of flavonoids was evaluated.

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Antioxidant and pro-oxidant actions of flavonoids: effects on DNA damage induced by nitric oxide, peroxynitrite and nitroxyl anion

Cited by 213 publications

References 38 publications

Tyrosine‐nitration of caspase 3 and cytochrome c does not suppress apoptosis induction in squamous cell carcinoma cells

Tyrosine‐nitration of caspase 3 and cytochrome c does not suppress apoptosis induction in squamous cell carcinoma cells

Biochemistry of Nitric Oxide

Voltammetric Detection of Antioxidative Properties of Flavonoids Using Electrically Heated DNA Modified Carbon Paste Electrode

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