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Journal articles on the topic 'Oxidative DNA damage'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

Skrypnyk, N. V., and O. O. Maslova. "Oxidative DNA damage." Biopolymers and Cell 23, no. 3 (2007): 202–14. http://dx.doi.org/10.7124/bc.000766.

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2

Hayes, Robert C., Lynn A. Petrullo, Haimei Huang, Susan S. Wallace, and J. Eugene LeClerc. "Oxidative damage in DNA." Journal of Molecular Biology 201, no. 2 (1988): 239–46. http://dx.doi.org/10.1016/0022-2836(88)90135-0.

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3

Collins, A. R., and E. Horváthová. "Oxidative DNA damage, antioxidants and DNA repair: applications of the comet assay." Biochemical Society Transactions 29, no. 2 (2001): 337–40. http://dx.doi.org/10.1042/bst0290337.

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Estimates of background levels of oxidative base damage in human white blood cells vary enormously, from 300 down to 0.4 molecules of 8-oxoguanine per 106 guanines. An EC-funded Concerted Action, the European Standards Committee on Oxidative DNA Damage, is currently attempting to resolve the discrepancy and to agree a realistic estimate of basal endogenous oxidation. Oxidation of lymphocyte DNA is a useful marker of oxidative stress, and this can be decreased by supplementation with pure antioxidants or with foods rich in antioxidants. The steady-state level of DNA oxidation is ultimately cont

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4

Soria-Meneses, Pedro Javier, Alejandro Jurado-Campos, Virgilio Gómez-Rubio, et al. "Determination of Ram (Ovis aries) Sperm DNA Damage Due to Oxidative Stress: 8-OHdG Immunodetection Assay vs. SCSA®." Animals 12, no. 23 (2022): 3286. http://dx.doi.org/10.3390/ani12233286.

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Conventional DNA analysis techniques can hardly detect DNA damage in ruminant spermatozoa due to high DNA compaction in these cells. Furthermore, these techniques cannot discriminate whether the damage is due to oxidative stress. The main purpose of this study was to evaluate the efficacy of two techniques for determining DNA damage in ovine sperm when the source of that damage is oxidative stress. Semen samples from twenty Manchega rams (Ovis aries) were collected and cryopreserved. After thawing, the samples were subjected to different levels of oxidative stress, and DNA oxidation was quanti

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5

Anderson, Andrew P., Xuemei Luo, William Russell, and Y. Whitney Yin. "Oxidative damage diminishes mitochondrial DNA polymerase replication fidelity." Nucleic Acids Research 48, no. 2 (2019): 817–29. http://dx.doi.org/10.1093/nar/gkz1018.

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Abstract Mitochondrial DNA (mtDNA) resides in a high ROS environment and suffers more mutations than its nuclear counterpart. Increasing evidence suggests that mtDNA mutations are not the results of direct oxidative damage, rather are caused, at least in part, by DNA replication errors. To understand how the mtDNA replicase, Pol γ, can give rise to elevated mutations, we studied the effect of oxidation of Pol γ on replication errors. Pol γ is a high fidelity polymerase with polymerase (pol) and proofreading exonuclease (exo) activities. We show that Pol γ exo domain is far more sensitive to ox

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6

Kwiatkowski, Dominik, Piotr Czarny, Monika Toma, et al. "Associations between DNA Damage, DNA Base Excision Repair Gene Variability and Alzheimer's Disease Risk." Dementia and Geriatric Cognitive Disorders 41, no. 3-4 (2016): 152–71. http://dx.doi.org/10.1159/000443953.

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Background: Increased oxidative damage to DNA is one of the pathways involved in Alzheimer's disease (AD). Insufficient base excision repair (BER) is in part responsible for increased oxidative DNA damage. The aim of the present study was to assess the effect of polymorphic variants of BER-involved genes and the peripheral markers of DNA damage and repair in patients with AD. Material and Methods: Comet assays and TaqMan probes were used to assess DNA damage, BER efﬁciency and polymorphic variants of 12 BER genes in blood samples from 105 AD patients and 130 controls. The DNA repair efficacy (

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7

Jeng, Hueiwang Anna, Chih-Hong Pan, Mu-Rong Chao, and Wen-Yi Lin. "Sperm DNA oxidative damage and DNA adducts." Mutation Research/Genetic Toxicology and Environmental Mutagenesis 794 (December 2015): 75–82. http://dx.doi.org/10.1016/j.mrgentox.2015.09.002.

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8

Guan, Zhe, Hongjie Song, and Rui Liu. "Adventures of DNA: Oxidative Damage." Daxue Huaxue 37, no. 9 (2022): 2204087–0. http://dx.doi.org/10.3866/pku.dxhx202299999.

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9

Takeuchi, Toru, Kanehisa Morimoto, Yasuhiro Nakaya, Naoki Kato, and Kunitomo Watanabe. "Oxidative DNA damage in anaerobes." Free Radical Biology and Medicine 25 (January 1998): S79. http://dx.doi.org/10.1016/s0891-5849(98)90254-4.

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10

Hartmann, A., and A. M. Niess. "Oxidative DNA damage in exercise." Pathophysiology 5 (June 1998): 112. http://dx.doi.org/10.1016/s0928-4680(98)80719-0.

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11

Ames, Bruce N. "Oxidative DNA damage and aging." Free Radical Biology and Medicine 9 (January 1990): 45. http://dx.doi.org/10.1016/0891-5849(90)90326-e.

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12

McCauley, Micah J., Leah Furman, Catherine A. Dietrich, et al. "DNA Stability after Oxidative Damage." Biophysical Journal 114, no. 3 (2018): 684a. http://dx.doi.org/10.1016/j.bpj.2017.11.3688.

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13

Pereira, Cristiana, Rosa Coelho, Daniela Grácio, et al. "DNA Damage and Oxidative DNA Damage in Inflammatory Bowel Disease." Journal of Crohn's and Colitis 10, no. 11 (2016): 1316–23. http://dx.doi.org/10.1093/ecco-jcc/jjw088.

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14

Karger, Stefan, Kerstin Krause, Cornelia Engelhardt, et al. "Distinct pattern of oxidative DNA damage and DNA repair in follicular thyroid tumours." Journal of Molecular Endocrinology 48, no. 3 (2012): 193–202. http://dx.doi.org/10.1530/jme-11-0119.

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Increased oxidative stress has been linked to thyroid carcinogenesis. In this paper, we investigate whether oxidative DNA damage and DNA repair differ in follicular adenoma (FA) and follicular thyroid carcinoma (FTC). 7,8-Dihydro-8-oxoguanine (8-OxoG) formation was analysed by immunohistochemistry in 46 FAs, 52 FTCs and 18 normal thyroid tissues (NTs). mRNA expression of DNA repair genes OGG1, Mut Y homologue (MUTYH) and endonuclease III (NTHL1) was analysed by real-time PCR in 19 FAs, 25 FTCs and 19 NTs. Induction and repair of oxidative DNA damage were studied in rat FRTL-5 cells after u.v.

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15

Toomey, Lillian M., Melissa G. Papini, Thomas O. Clarke, et al. "Secondary Degeneration of Oligodendrocyte Precursor Cells Occurs as Early as 24 h after Optic Nerve Injury in Rats." International Journal of Molecular Sciences 24, no. 4 (2023): 3463. http://dx.doi.org/10.3390/ijms24043463.

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Optic nerve injury causes secondary degeneration, a sequela that spreads damage from the primary injury to adjacent tissue, through mechanisms such as oxidative stress, apoptosis, and blood-brain barrier (BBB) dysfunction. Oligodendrocyte precursor cells (OPCs), a key component of the BBB and oligodendrogenesis, are vulnerable to oxidative deoxyribonucleic acid (DNA) damage by 3 days post-injury. However, it is unclear whether oxidative damage in OPCs occurs earlier at 1 day post-injury, or whether a critical ‘window-of-opportunity’ exists for therapeutic intervention. Here, a partial optic ne

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16

Hanna, Bishoy M. F., Maurice Michel, Thomas Helleday, and Oliver Mortusewicz. "NEIL1 and NEIL2 Are Recruited as Potential Backup for OGG1 upon OGG1 Depletion or Inhibition by TH5487." International Journal of Molecular Sciences 22, no. 9 (2021): 4542. http://dx.doi.org/10.3390/ijms22094542.

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DNA damage caused by reactive oxygen species may result in genetic mutations or cell death. Base excision repair (BER) is the major pathway that repairs DNA oxidative damage in order to maintain genomic integrity. In mammals, eleven DNA glycosylases have been reported to initiate BER, where each recognizes a few related DNA substrate lesions with some degree of overlapping specificity. 7,8-dihydro-8-oxoguanine (8-oxoG), one of the most abundant DNA oxidative lesions, is recognized and excised mainly by 8-oxoguanine DNA glycosylase 1 (OGG1). Further oxidation of 8-oxoG generates hydantoin lesio

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17

Ávalos, A., A. I. Haza, and Paloma Morales. "Manufactured Silver Nanoparticles of Different Sizes Induced DNA Strand Breaks and Oxidative DNA Damage in Hepatoma and Leukaemia Cells and in Dermal and Pulmonary Fibroblasts." Folia Biologica 61, no. 1 (2015): 33–42. http://dx.doi.org/10.14712/fb2015061010033.

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Many classes of silver nanoparticles (AgNPs) have been synthesized and widely applied, but no conclusive information on their potential cytotoxicity and genotoxicity mechanisms is available. Therefore, the purpose of this study was to compare the potential genotoxic effects (DNA strand breaks and oxidative DNA damage) of 4.7 nm coated and 42 nm uncoated AgNPs, using the comet assay, in four relevant human cell lines (hepatoma, leukaemia, and dermal and pulmonary fibroblasts) in order to understand the impact of such nanomaterials on cellular DNA. The results indicated that in all cell lines te

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18

Kanvah, Sriram, and Gary B. Schuster. "Oxidative damage to DNA: Inhibition of guanine damage." Pure and Applied Chemistry 78, no. 12 (2006): 2297–304. http://dx.doi.org/10.1351/pac200678122297.

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One-electron oxidation of DNA results in chemical damage to nucleobases, particularly guanine in multiple G sequences. Oxidation may be triggered by numerous events, including photosensitization. We describe studies of photoinduced oxidations of DNA triggered by irradiation of covalently linked anthraquinone derivatives under various conditions that affect the global structure of the DNA. These structural changes have subtle effects on the result of the one-electron oxidation.

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19

Tripathi, Diwaker, Delene J. Oldenburg, and Arnold J. Bendich. "Oxidative and Glycation Damage to Mitochondrial DNA and Plastid DNA during Plant Development." Antioxidants 12, no. 4 (2023): 891. http://dx.doi.org/10.3390/antiox12040891.

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Oxidative damage to plant proteins, lipids, and DNA caused by reactive oxygen species (ROS) has long been studied. The damaging effects of reactive carbonyl groups (glycation damage) to plant proteins and lipids have also been extensively studied, but only recently has glycation damage to the DNA in plant mitochondria and plastids been reported. Here, we review data on organellar DNA maintenance after damage from ROS and glycation. Our focus is maize, where tissues representing the entire range of leaf development are readily obtained, from slow-growing cells in the basal meristem, containing

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20

Zhang, Weiran, Ranwei Zhong, Xiangping Qu, Yang Xiang, and Ming Ji. "Effect of 8-Hydroxyguanine DNA Glycosylase 1 on the Function of Immune Cells." Antioxidants 12, no. 6 (2023): 1300. http://dx.doi.org/10.3390/antiox12061300.

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Excess reactive oxygen species (ROS) can cause an imbalance between oxidation and anti-oxidation, leading to the occurrence of oxidative stress in the body. The most common product of ROS-induced base damage is 8-hydroxyguanine (8-oxoG). Failure to promptly remove 8-oxoG often causes mutations during DNA replication. 8-oxoG is cleared from cells by the 8-oxoG DNA glycosylase 1 (OGG1)-mediated oxidative damage base excision repair pathway so as to prevent cells from suffering dysfunction due to oxidative stress. Physiological immune homeostasis and, in particular, immune cell function are vulne

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21

III, David M. Wilson. "Repair mechanisms for oxidative DNA damage." Frontiers in Bioscience 8, no. 4 (2003): d963–981. http://dx.doi.org/10.2741/1109.

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22

Hirano, Takeshi. "Alcohol Consumption and Oxidative DNA Damage." International Journal of Environmental Research and Public Health 8, no. 7 (2011): 2895–906. http://dx.doi.org/10.3390/ijerph8072895.

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23

Loft, Steffen, Xin-Sheng Deng, Jingsheng Tuo, Anja Wellejus, Mette Sørensen, and Henrik E. Poulsen. "Experimental study of oxidative DNA damage." Free Radical Research 29, no. 6 (1998): 525–39. http://dx.doi.org/10.1080/10715769800300571.

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24

Lewis, J. G., and D. O. Adams. "Inflammation, oxidative DNA damage, and carcinogenesis." Environmental Health Perspectives 76 (December 1987): 19–27. http://dx.doi.org/10.1289/ehp.877619.

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25

Nguyen, Anh L., and James A. Imlay. "What reductant drives oxidative DNA damage?" Free Radical Biology and Medicine 25 (January 1998): S76. http://dx.doi.org/10.1016/s0891-5849(98)90242-8.

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26

D'Incà, R., R. Cardin, S. Bortolan, et al. "Oxidative DNA damage in ulcerative colitis." Digestive and Liver Disease 32 (May 2000): A12. http://dx.doi.org/10.1016/s1590-8658(00)80091-2.

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27

Lee, S. "Oxidative DNA Damage and Cardiovascular Disease." Trends in Cardiovascular Medicine 11, no. 3-4 (2001): 148–55. http://dx.doi.org/10.1016/s1050-1738(01)00094-9.

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28

D’Inca’, Renata, Romilda Cardin, Antonio Ferronato, et al. "Oxidative DNA damage in ulcerative colitis." Gastroenterology 118, no. 4 (2000): A1121. http://dx.doi.org/10.1016/s0016-5085(00)80292-9.

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29

Milligan, Jamie R., Nancy Q. Tran, Anne Ly, and John F. Ward. "Peptide Repair of Oxidative DNA Damage†." Biochemistry 43, no. 17 (2004): 5102–8. http://dx.doi.org/10.1021/bi030232l.

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30

Martinez, G. "Oxidative and alkylating damage in DNA." Mutation Research/Reviews in Mutation Research 544, no. 2-3 (2003): 115–27. http://dx.doi.org/10.1016/j.mrrev.2003.05.005.

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31

Barzilai, Ari, and Ken-Ichi Yamamoto. "DNA damage responses to oxidative stress." DNA Repair 3, no. 8-9 (2004): 1109–15. http://dx.doi.org/10.1016/j.dnarep.2004.03.002.

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32

Daniel, Lambert N., Yan Mao, and Saffiotti Umberto. "Oxidative DNA damage by crystalline silica." Free Radical Biology and Medicine 14, no. 5 (1993): 463–72. http://dx.doi.org/10.1016/0891-5849(93)90103-2.

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33

Retèl, Jan, Barbara Hoebee, Jacqueline E. F. Braun, et al. "Mutational specificity of oxidative DNA damage." Mutation Research/Genetic Toxicology 299, no. 3-4 (1993): 165–82. http://dx.doi.org/10.1016/0165-1218(93)90094-t.

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34

Suliman, Hagir B., Martha S. Carraway, and Claude A. Piantadosi. "Postlipopolysaccharide Oxidative Damage of Mitochondrial DNA." American Journal of Respiratory and Critical Care Medicine 167, no. 4 (2003): 570–79. http://dx.doi.org/10.1164/rccm.200206-518oc.

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35

Tzortzaki, Eleni G., Katerina Dimakou, Eirini Neofytou, et al. "Oxidative DNA Damage and Somatic Mutations." Chest 141, no. 5 (2012): 1243–50. http://dx.doi.org/10.1378/chest.11-1653.

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36

Umegaki, Keizo. "Antioxidative Nutrients and Oxidative DNA Damage." Japanese Journal of Nutrition and Dietetics 62, no. 2 (2004): 65–72. http://dx.doi.org/10.5264/eiyogakuzashi.62.65.

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37

Teebor, G. W., R. J. Boorstein, and S. V. Cannon. "Enzymatic Repair of Oxidative DNA Damage." Free Radical Research Communications 6, no. 2-3 (1989): 185–87. http://dx.doi.org/10.3109/10715768909073466.

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38

Eriksson, Ulf J. "Oxidative DNA damage and embryo development." Nature Medicine 5, no. 7 (1999): 715. http://dx.doi.org/10.1038/10420.

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39

Chubatsu, L. S., and R. Meneghini. "Metallothionein protects DNA from oxidative damage." Biochemical Journal 291, no. 1 (1993): 193–98. http://dx.doi.org/10.1042/bj2910193.

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Metallothionein (MT) is a potent hydroxyl radical scavenger but its antioxidant properties in vivo have not been defined. Most of the recent results indicate that it does not afford protection to cells against the lethal action of oxidative stress. However, the possibility that MT confers protection against oxidative damage to a specific cellular target, such as DNA, had not been considered. We compared V79 Chinese hamster cells enriched in and depleted of MT in terms of DNA-strand scission. Zinc induces an increase in MT content of V79 Chinese hamster cells, without concomitant increase in th

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40

Van Remmen, Holly, Michelle L. Hamilton, and A. Richardson. "Oxidative Damage to DNA and Aging." Exercise and Sport Sciences Reviews 31, no. 3 (2003): 149–53. http://dx.doi.org/10.1097/00003677-200307000-00009.

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41

Anson, R. Michael, and Vilhelm A. Bohr. "Mitochondria, oxidative DNA damage, and aging." AGE 23, no. 4 (2000): 199–218. http://dx.doi.org/10.1007/s11357-000-0020-y.

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42

Collins, Andrew R. "Oxidative DNA damage, antioxidants, and cancer." BioEssays 21, no. 3 (1999): 238–46. http://dx.doi.org/10.1002/(sici)1521-1878(199903)21:3<238::aid-bies8>3.0.co;2-3.

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43

Bendesky, Andrés, Alejandra Michel, Monserrat Sordo, et al. "DNA damage, oxidative mutagen sensitivity, and repair of oxidative DNA damage in nonmelanoma skin cancer patients." Environmental and Molecular Mutagenesis 47, no. 7 (2006): 509–17. http://dx.doi.org/10.1002/em.20220.

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44

Poulsen, Henrik E., Allan Weimann, and Steffen Loft. "Methods to detect DNA damage by free radicals: relation to exercise." Proceedings of the Nutrition Society 58, no. 4 (1999): 1007–14. http://dx.doi.org/10.1017/s0029665199001329.

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Epidemiological investigations repeatedly show decreased morbidity from regular exercise compared with sedentary life. A large number of investigations have demonstrated increased oxidation of important cellular macromolecules, whereas other investigators have found no effects or even signs of lowering of oxidation of macromolecules. In particular, extreme and long-duration strenuous exercise appears to lead to deleterious oxidation of cellular macromolecules. The oxidation of DNA is important because the oxidative modifications of DNA bases, particularly the 8-hydroxylation of guanine, are mu

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45

Loft, Steffen, Pernille Høgh Danielsen, Lone Mikkelsen, Lotte Risom, Lykke Forchhammer, and Peter Møller. "Biomarkers of oxidative damage to DNA and repair." Biochemical Society Transactions 36, no. 5 (2008): 1071–76. http://dx.doi.org/10.1042/bst0361071.

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Oxidative-stress-induced damage to DNA includes a multitude of lesions, many of which are mutagenic and have multiple roles in cancer and aging. Many lesions have been characterized by MS-based methods after extraction and digestion of DNA. These preparation steps may cause spurious base oxidation, which is less likely to occur with methods such as the comet assay, which are based on nicking of the DNA strand at modified bases, but offer less specificity. The European Standards Committee on Oxidative DNA Damage has concluded that the true levels of the most widely studied lesion, 8-oxodG (8-ox

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46

Lettieri, Gennaro, Giovanni D’Agostino, Elena Mele, et al. "Discovery of the Involvement in DNA Oxidative Damage of Human Sperm Nuclear Basic Proteins of Healthy Young Men Living in Polluted Areas." International Journal of Molecular Sciences 21, no. 12 (2020): 4198. http://dx.doi.org/10.3390/ijms21124198.

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DNA oxidative damage is one of the main concerns being implicated in severe cell alterations, promoting different types of human disorders and diseases. For their characteristics, male gametes are the most sensitive cells to the accumulation of damaged DNA. We have recently reported the relevance of arginine residues in the Cu(II)-induced DNA breakage of sperm H1 histones. In this work, we have extended our previous findings investigating the involvement of human sperm nuclear basic proteins on DNA oxidative damage in healthy males presenting copper and chromium excess in their semen. We found

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47

Rashki Ghaleno, Leila, AliReza Alizadeh, Joël R. Drevet, Abdolhossein Shahverdi, and Mojtaba Rezazadeh Valojerdi. "Oxidation of Sperm DNA and Male Infertility." Antioxidants 10, no. 1 (2021): 97. http://dx.doi.org/10.3390/antiox10010097.

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One important reason for male infertility is oxidative stress and its destructive effects on sperm structures and functions. The particular composition of the sperm membrane, rich in polyunsaturated fatty acids, and the easy access of sperm DNA to oxidative damage due to sperm cell specific cytologic and metabolic features (no cytoplasm left and cells unable to mount stress responses) make it the cell type in metazoans most susceptible to oxidative damage. In particular, oxidative damage to the spermatozoa genome is an important issue and a cause of male infertility, usually associated with si

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48

Kong, Qingjun, Qingzhi Zeng, Jia Yu, Hongxi Xiao, Jun Lu, and Xueyan Ren. "Mechanism of Resveratrol Dimers Isolated from Grape Inhibiting 1O2 Induced DNA Damage by UHPLC-QTOF-MS2 and UHPLC-QQQ-MS2 Analyses." Biomedicines 9, no. 3 (2021): 271. http://dx.doi.org/10.3390/biomedicines9030271.

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Resveratrol dimers have been extensively reported on due to their antioxidative activity. Previous studies revealed that resveratrol dimer has been shown to selectively quench singlet oxygen (1O2), and could protect DNA from oxidative damage. The mechanism of resveratrol dimers protecting DNA against oxidative damage is still not clear. Therefore, in this project, the reactants and products of resveratrol dimers protecting guanine from oxidative damage were qualitatively monitored and quantitatively analyzed by UHPLC-QTOF-MS2 and UHPLC-QQQ-MS2. Results showed that when guanine and resveratrol

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49

Sirotová, Ľudmila, and Marcela Matulová. "DNA damage by oxidized fatty acids detected by DNA/SPE biosensor." Nova Biotechnologica et Chimica 8, no. 1 (2021): 45–53. http://dx.doi.org/10.36547/nbc.1307.

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Electrochemical DNA/screen-printed electrode biosensor (DNA/SPE biosensor) was tested for the detection of alterations in DNA formed as a consequence of the reaction between DNA and oxidative products of fatty acids. Interaction of DNA with a mixture of products generated during the oxidation of linoleic and oleic acids manifested DNA damage depending on a tested fatty acid and the presence of hydroperoxides and thiobarbituric acid reactive substances (TBARS) determined after the oxidation of fatty acids. A bigger extent of the DNA damage was registered in the case of the interaction with oxid

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50

Szeto, Yim Tong. "Eosinophilia and Leucocytic DNA damage." F1000Research 13 (October 11, 2024): 1216. http://dx.doi.org/10.12688/f1000research.157145.1.

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Eosinophilia serves as an indicator of allergy and parasite infestation. Eosinophil granules are believed to have adverse effects on cells and contribute to oxidative stress. In our current study, we investigated the relationship between eosinophilia and healthy subjects in terms of nuclear DNA damage in peripheral leukocytes. The comet assay was employed to test whole blood samples from 52 subjects in each group. The results revealed that eosinophilia subjects exhibited significantly higher levels of nuclear DNA damage in leukocytes compared to healthy subjects. Additionally, a weak positive

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