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We began analyzing https://www.degruyterbrill.com/document/doi/10.1515/BC.2002.098/html, but it redirected us to https://www.degruyterbrill.com/document/doi/10.1515/BC.2002.098/html. The analysis below is for the second page.

Title[redir]:
Exocyclic DNA Adducts as Oxidative Stress Markers in Colon Carcinogenesis: Potential Role of Lipid Peroxidation, Dietary Fat and Antioxidants
Description:
Molecular pathways to colorectal cancer involve multiple genetic changes, whereby extensive oxyradical damage causes mutations in cancerrelated genes and leads to a cycle of cell death and regeneration. Besides direct oxidative DNAdamage, reactive oxygen and nitrogen species can induce etheno ()DNA adducts mainly via trans-4-hydroxy-2-nonenal, generated as the major aldehyde by lipid peroxidation (LPO) of ω-6 PUFAs. Patients with familial adenomatous polyposis (FAP) develop multiple colorectal adenomas. In affected tissues increased LPO could be triggered due to increased arachidonic acid metabolism as a result of elevated cyclooxygenases. Our studies demonstrated an increased DNA adduct level in affected colon epithelia of FAP patients. DNA adducts are promutagenic and can cause genomic instability that drives colorectal adenoma to malignancy. We have further investigated the potential chemopreventive properties of olive oil and its polyphenolic components. Mediterranean diet, of which olive oil is a major fatty acid source, has protective effects against human breast and colorectal cancers. Olive oil extracts and the newly identified lignan fractions showed high antioxidant capacity in vitro. As DNA adducts are biomarkers for oxidative stress and LPO induced DNA damage, they can verify the efficacy of newly identified antioxidants, e.g. from olive oil, as chemopreventive agents against colon carcinogenesis.

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Keywords {🔍}

dna, adducts, oxidative, colon, carcinogenesis, stress, potential, lipid, peroxidation, antioxidants, colorectal, olive, oil, human, content, search, exocyclic, markers, role, dietary, fat, published, gruyter, journal, cancer, damage, lpo, increased, acid, access, protein, article, author, brill, issue, molecular, multiple, major, patients, fap, affected, level, chemopreventive, properties, cancers, newly, identified, repair, analysis, methylation,

Topics {✒️}

newly identified antioxidants dna repair glycosylases search journal search exocyclic dna adducts cancer recent aspects oxidative dna damage antioxidants dna polymorphisms drives colorectal adenoma ceramide level alters human transferrin receptor extensive oxyradical damage affected colon epithelia antioxidants helmut bartsch trans-4-hydroxy-2-nonenal familial adenomatous polyposis yeast msh2-msh6 conditions legal notice direct oxidative dnadamage potential chemopreventive properties oxidative stress markers mammalian genomes methylation newsletter institutional access olive oil extracts colorectal cancers owen published/copyright dna adducts issue highlight dna methylation journal https prion protein oxidative stress human breast privacy policy colon carcinogenesis major aldehyde author olive oil chemopreventive agents potential role subjects services lipid peroxidation dietary fat jagadeesan nair cancerrelated genes cell death reactive oxygen nitrogen species induce etheno ω-6 pufas triggered due

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Schema {🗺️}

Article:
      author:
            type:Person
            name:Helmut Bartsch
            type:Person
            name:Jagadeesan Nair
            type:Person
            name:Robert W. Owen
      editor:
      audience:
      datePublished:2002-06-26
      headline:
      keywords:
      isAccessibleForFree:
      publisher:
         type:Organization
         name:De Gruyter
      context:https://schema.org
      name:Exocyclic DNA Adducts as Oxidative Stress Markers in Colon Carcinogenesis: Potential Role of Lipid Peroxidation, Dietary Fat and Antioxidants
      image:https://www.degruyterbrill.com/document/cover/journal_key/BCHM/thumbnail
      url:https://doi.org/10.1515/BC.2002.098
Person:
      name:Helmut Bartsch
      name:Jagadeesan Nair
      name:Robert W. Owen
Organization:
      name:De Gruyter

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