Low doses of selenium specifically stimulate the repair of oxidative DNA damage in LNCaP prostate cancer cells (1582 views)
Free Radic Res Free Radical Research (ISSN: 1071-5762), 2012; 46(2): 105-115.
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Paper type: Journal Article,
Impact factor: 3.279, 5-year impact factor: 2.836
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-84856283957&partnerID=40&md5=9d7fa5fb9a4c038dfdf902a99acff4f0
Keywords: Comet Assay, Dna Repair, Hogg1, Oxidative Dna Damage, Selenium, Hydrogen Peroxide, Methylmethane Sulfonate, Selenomethionine, Sodium Selenite, Unclassified Drug, Antineoplastic Activity, Antioxidant Activity, Article, Cell Strain Lncap, Cell Viability, Controlled Study, Cytotoxicity, Drug Effect, Genotoxicity, Human, Human Cell, Low Drug Dose, Molecular Mechanics, Oxidative Stress, Prostate Adenocarcinoma, Treatment Response, Ultraviolet A Radiation, Anticarcinogenic Agents, Cell Line, Tumor, Cell Survival, Deoxyguanosine, Dna Fragmentation, Glutathione Peroxidase, Oxidation-Reduction, Prostatic Neoplasms, Thioredoxin-Disulfide Reductase, Ultraviolet Rays,
Affiliations:
*** IBB - CNR ***
Laboratoire des L é Sions des Acides Nucl é Iques, SCIB, INAC, 17 rue des Martyrs, Grenoble Cedex 9, F-38054, France
Hacettepe University, Faculty of Pharmacy, Department of Toxicology, 06100 Ankara, Turkey
University of Illinois at Chicago, Department of Pathology, 840 South Wood, Chicago, IL, United States
References:
Not available.
Free Radic Res Free Radical Research (ISSN: 1071-5762), 2012; 46(2): 105-115.
Export to BibTeX Export to EndNote
Paper type: Journal Article,
Impact factor: 3.279, 5-year impact factor: 2.836
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-84856283957&partnerID=40&md5=9d7fa5fb9a4c038dfdf902a99acff4f0
Keywords: Comet Assay, Dna Repair, Hogg1, Oxidative Dna Damage, Selenium, Hydrogen Peroxide, Methylmethane Sulfonate, Selenomethionine, Sodium Selenite, Unclassified Drug, Antineoplastic Activity, Antioxidant Activity, Article, Cell Strain Lncap, Cell Viability, Controlled Study, Cytotoxicity, Drug Effect, Genotoxicity, Human, Human Cell, Low Drug Dose, Molecular Mechanics, Oxidative Stress, Prostate Adenocarcinoma, Treatment Response, Ultraviolet A Radiation, Anticarcinogenic Agents, Cell Line, Tumor, Cell Survival, Deoxyguanosine, Dna Fragmentation, Glutathione Peroxidase, Oxidation-Reduction, Prostatic Neoplasms, Thioredoxin-Disulfide Reductase, Ultraviolet Rays,
Affiliations:
*** IBB - CNR ***
Laboratoire des L é Sions des Acides Nucl é Iques, SCIB, INAC, 17 rue des Martyrs, Grenoble Cedex 9, F-38054, France
Hacettepe University, Faculty of Pharmacy, Department of Toxicology, 06100 Ankara, Turkey
University of Illinois at Chicago, Department of Pathology, 840 South Wood, Chicago, IL, United States
References:
Not available.
Low doses of selenium specifically stimulate the repair of oxidative DNA damage in LNCaP prostate cancer cells
Epidemiological studies have demonstrated an inverse relationship between selenium (Se) intake and cancer incidence and/or mortality. However, the molecular mechanisms underlying the cancer chemopreventive activity of Se compounds remain largely unknown. The objective of this study was to investigate the effect of low doses of Se on the stimulation of DNA repair systems in response to four different qualities of DNA damage. P53-proficient LNCaP human prostate adenocarcinoma cells were grown either untreated or in the presence of low concentrations of two Se compounds (30° nM sodium selenite, or 10μM selenomethionine) and exposed to UVA, H 2O 2, methylmethane sulfonate (MMS) or UVC. Cell viability as well as DNA damage induction and repair were evaluated by the alkaline Comet assay. Overall, Se was shown to be a very potent protector against cell toxicity and genotoxicity induced by oxidative stress (UVA or H 2O 2) but not from the agents that induce other types of deleterious lesions (MMS or UVC). Furthermore, Se-treated cells exhibited increased oxidative DNA repair activity, indicating a novel mechanism of Se action. Therefore, the benefits of Se could be explained by a combination of antioxidant activity, the reduction in DNA damage and the enhancement of oxidative DNA repair capacity. © 2012 Informa UK, Ltd.
Epidemiological studies have demonstrated an inverse relationship between selenium (Se) intake and cancer incidence and/or mortality. However, the molecular mechanisms underlying the cancer chemopreventive activity of Se compounds remain largely unknown. The objective of this study was to investigate the effect of low doses of Se on the stimulation of DNA repair systems in response to four different qualities of DNA damage. P53-proficient LNCaP human prostate adenocarcinoma cells were grown either untreated or in the presence of low concentrations of two Se compounds (30° nM sodium selenite, or 10μM selenomethionine) and exposed to UVA, H 2O 2, methylmethane sulfonate (MMS) or UVC. Cell viability as well as DNA damage induction and repair were evaluated by the alkaline Comet assay. Overall, Se was shown to be a very potent protector against cell toxicity and genotoxicity induced by oxidative stress (UVA or H 2O 2) but not from the agents that induce other types of deleterious lesions (MMS or UVC). Furthermore, Se-treated cells exhibited increased oxidative DNA repair activity, indicating a novel mechanism of Se action. Therefore, the benefits of Se could be explained by a combination of antioxidant activity, the reduction in DNA damage and the enhancement of oxidative DNA repair capacity. © 2012 Informa UK, Ltd.
Low doses of selenium specifically stimulate the repair of oxidative DNA damage in LNCaP prostate cancer cells
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Low doses of selenium specifically stimulate the repair of oxidative DNA damage in LNCaP prostate cancer cells
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View Export to BibTeX Export to EndNote
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Impact Factor: 4.823
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Impact Factor: 3.078
View Export to BibTeX Export to EndNote
Minopoli G, Stante M, Napolitano F, Telese F, Aloia L, De Felice M, Di Lauro R, Pacelli R, Brunetti A, Zambrano N, Russo T
* Essential roles for Fe65, Alzheimer amyloid precursor-binding protein, in the cellular response to DNA damage (1166 views)
Jbc Papers (ISSN: 0021-9258, 1083-351x, 0021-9258linking), 2007 Jan 12; 282(2): 831-835.
Impact Factor: 5.581
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Limauro D, Pedone E, Pirone L, Bartolucci S
* Identification and characterization of 1-Cys peroxiredoxin from Sulfolobus solfataricus and its involvement in the response to oxidative stress (685 views)
Febs Journal (ISSN: 1742-464x), 2006 Feb; 273(4): 721-731.
Impact Factor: 3.033
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Copani A, Hoozemans JJM, Caraci F, Calafiore M, Van Haastert ES, Veerhuis R, Rozemuller AJM, Aronica E, Sortino MA, Nicoletti F
* Dna Polymerase-Beta Is Expressed Early In Neurons Of Alzheimer'S Disease Brain And Is Loaded Into Dna Replication Forks In Neurons Challenged With Beta-Amyloid (1036 views)
J Neurosci (ISSN: 0270-6474, 0361-803x, 1529-2401), 2006; 26(43): 10949-10957.
Impact Factor: 2.117
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Pedone E, Bartolucci S, Fiorentino G
* Sensing and adapting to environmental stress: The Archaeal tactic (598 views)
Frontiers In Bioscience (ISSN: 1093-9946, 1093-4715), 2004 Sep 1; 9: 2909-2926.
Impact Factor: 3.226
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Tedesco I, Russo GL, Nazzaro F, Russo M, Palumbo R
* Antioxidant effect of red wine anthocyanins in normal and catalase-inactive human erythrocytes (1664 views)
J Nutr Biochem (ISSN: 0955-2863), 2001 Sep; 12(9): 505-511.
Impact Factor: 1.039
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Tabbì G, Fry SC, Bonomo RP
ESR study of the non-enzymic scission of xyloglucan by an ascorbate-H2O2-copper system: The involvement of the hydroxyl radical and the degradation of ascorbate (561 views)
J Chem Res (ISSN: 0162-0134, 1873-3344, 0162-0134print), 2001 Apr; 84(3-4): 179-187.
Impact Factor: 1.729
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Tedesco I, Russo M, Russo P, Iacomino G, Russo GL, Carraturo A, Faruolo C, Moio L, Palumbo R
Antioxidant effect of red wine polyphenols on red blood cells (1181 views)
J Nutr Biochem (ISSN: 0955-2863), 2000 Feb; 11(2): 114-119.
Impact Factor: 1.083
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Herscher LL, Cook JA, Pacelli R, Pass HI, Russo A, Mitchell JB
Principles of chemoradiation: Theoretical and practical considerations (817 views)
Oncology (ISSN: 0890-9091), 1999 Oct; 13(10SUPPL.5): 11-22.
Impact Factor: 0.933
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Cook JA, Krishna MC, Pacelli R, DeGraff W, Liebmann J, Mitchell JB, Russo A, Wink DA
Nitric oxide enhancement of melphalan-induced cytotoxicity (805 views)
Br J Cancer (ISSN: 0007-0920, 0007-0920print, 0007-0920linking), 1997 Sep; 76(3): 325-334.
Impact Factor: 2.938
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Wink DA, Cook JA, Pacelli R, DeGraff W, Gamson J, Liebmann J, Krishna MC, Mitchell JB
The effect of various nitric oxide-donor agents on hydrogen peroxide-mediated toxicity: A direct correlation between nitric oxide formation and protection (1177 views)
Arch Bioch Bioph (ISSN: 0003-9861, 0003-9861linking), 1996 Jul 15; 331(2): 241-248.
Impact Factor: 2.649
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Pacelli R, Taira J, Cook JA, Wink DA, Krishna MC
Hydroxyurea reacts with heme proteins to generate nitric oxide [6] (611 views)
Lancet (ISSN: 0140-6736), 1996 Mar 30; 347(9005): 900-900.
Impact Factor: 16.135
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Wink DA, Cook JA, Pacelli R, Liebmann J, Krishna MC, Mitchell JB
Nitric oxide (NO) protects against cellular damage by reactive oxygen species (971 views)
Toxicology Letters (ISSN: 0378-4274), 1995 Dec; 82-3: 221-226.
Impact Factor: 1.128
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Bonomo RP, Marchelli R, Tabbì G
Study of H2O2 interaction with copper(II) complexes with diamino-diamide type ligands, diastereoisomeric dipeptides, and tripeptides (762 views)
J Chem Res (ISSN: 0162-0134, 1873-3344, 0162-0134print), 1995 Nov 15; 60(3): 205-218.
Impact Factor: 1.342
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Pacelli R, Wink DA, Cook JA, Krishna MC, DeGraff W, Friedman N, Tsokos M, Samuni A, Mitchell JB
NITRIC-OXIDE POTENTIATES HYDROGEN PEROXIDE-INDUCED KILLING OF ESCHERICHIA-COLI (1111 views)
Journal Of Experimental Medicine (ISSN: 0022-1007), 1995 Nov 1; 182(5): 1469-1479.
Impact Factor: 14.384
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Condorelli G, Costanzo LL, De Guidi G, Giuffrida S, Rizzarelli E, Vecchio G
INHIBITION OF PHOTOHEMOLYSIS BY COPPER(II) COMPLEXES WITH SOD-LIKE ACTIVITY (688 views)
J Chem Res (ISSN: 0162-0134, 1873-3344, 0162-0134print), 1994 Jun; 54(4): 257-265.
Impact Factor: 1.342
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34 Records (32 excluding Abstracts).
Total impact factor: 142.244 (122.379 excluding Abstracts).
Total 5 year impact factor: 166.986 (138.541 excluding Abstracts).
Total impact factor: 142.244 (122.379 excluding Abstracts).
Total 5 year impact factor: 166.986 (138.541 excluding Abstracts).
1582 views. Last view on Saturday 26 April 2025, 1:32:00
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