Oxyradicals and DNA damage.

By L. Marnett. Carcinogenesis, 2000

1,922 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/3e52dab2d615c67a27c9f8dc49409a728fdedf25

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Citations in the corpus

Chemical and molecular mechanisms of antioxidants: experimental approaches and model systems (2009, background): “Lipid peroxidation and DNA damage are associated with a variety of chronic health problems, such as cancer, ageing and atherosclerosis [109–111].”
Reactive oxygen species, antioxidants, and the mammalian thioredoxin system. (2001, background): “This mechanism may partly explain the high prevalence of cancer in individuals exposed to oxidative stress [3,37].”
Heavy Metals Toxicity and the Environment (2012, background): “Although mutations of DNA, which can activate oncogenesis or inhibit tumor suppression, were traditionally thought to be crucial factors for the initiation of carcinogenesis, recent studies have demonstrated that other molecular events, such as transcription activation, signal transduction, oncogene”
Role of oxygen radicals in DNA damage and cancer incidence (2004, background): “However, misrepair of DNA damage could result in mutations such as base substitution and deletion, also leading to carcinogenesis [75, 76].”
Oxidative stress, aging, and diseases (2018, background): “In particular, ROSinduced DNA damages can result in transcriptional arrest or induction/replication errors, or genomic instability, which are all associated with carcinogenesis.(65) Among oxidizedDNA products, 8-oxodG and 8-nitroguanine are considered biomarkers for inflammation-induced carcinogenes”
Biological functions of antioxidants in plant transformation (2008, background): “Excessive production of ROS often leads to oxidative stress, loss of cell function, and ultimately apoptosis or necrosis by its interference with various biomolecules, including proteins, lipids, and DNA (Marnett 2000).”
Chronic inflammation and oxidative stress in human carcinogenesis (2007, background): “In addition, hydroxypropanodeoxyguanosines are present in human DNA in presence of cancer.(41) These adducts are most probably derived from the reaction of DNA with acrolein and crotonaldehyde generated by the lipid peroxidation process.”
Necrosis, a well-orchestrated form of cell demise: signalling cascades, important mediators and concomitant immune response. (2006, background): “Sustained activation of both p38 MAPK and JNK is observed following treatment of MEF cells with the DNAalkylating agent N-methyl-N′-nitro-N-nitrosoguanidine (MNNG).”
Free Radicals: Properties, Sources, Targets, and Their Implication in Various Diseases (2014, background): “Most importantly, the excess ROS can damage the integrity of various biomolecules including lipids [13], proteins [14] and DNA [15] leading to increased oxidative stress in various human diseases such as diabetes mellitus, neurodegenerative diseases, rheumatoid arthritis, cataracts, cardiovascular d”
Chronic inflammation and cancer. (2002, background): “[42] Proneoplastic Mechanisms—Our best understanding of the proneoplastic activity of reactive oxygen and nitrogen intermediates comes from their ability to induce damage to DNA.[43,44] Exposure of cells to activated phagocytes leads to oxidative and nitrosative modification of bases, and single-str”
Inflammation and cancer IV. Colorectal cancer in inflammatory bowel disease: the role of inflammation. (2004, background): “How then might oxidative stress contribute to colorectal carcinogenesis? Free radicals have the potential to affect a large array of metabolic processes, because their targets include DNA, RNA, proteins, and lipids (44, 53).”
A review of the interaction among dietary antioxidants and reactive oxygen species. (2007, background): “Genetic alterations Mutagenic alteration of DNA is an initiating event in carcinogenesis, and mutations affecting gene expression and/or function, particularly those of tumor suppressor genes and proto-oncogenes; this can lead to unregulated growth typical of cancer cells [49].”