title: Genomic damage in end-stage renal failure: potential involvement of advanced glycation end products and carbonyl stress.
abstract: In patients with chronic renal failure, genomic damage has been shown by numerous biomarkers, such as micronuclei frequency and comet assay (single-cell gel electrophoresis) in peripheral lymphocytes, 8-hydroxy 2'-deoxyguanosine (8-OH-dG) content in leukocytes, mitochondrial DNA deletions in skeletal muscle tissue and hair follicles, as well as in DNA repair mechanisms in freshly isolated lymphocytes after ultraviolet light exposure. In the pathogenesis of DNA damage--besides genetic influences, enhanced reactive oxygen species (ROS), and lipid peroxidation-the genotoxic potential of advanced glycation end products (AGEs) and reactive carbonyl compounds deserve special attention. In fact, reactions of glucose with DNA can lead to mutagenic DNA AGEs. In vitro, incubation of tubulus cells with various AGEs and methylglyoxal induces DNA damage, which is suppressed by antioxidants. This underlines the role played by oxidative stress in DNA damage.
authors.affiliation: Institute of Pharmacology and Toxicology, University of Würzburg, Germany.
authors.forename: Helga
authors.initials: H
authors.lastname: Stopper
authors.forename: Nicole
authors.initials: N
authors.lastname: Schupp
authors.forename: Udo
authors.initials: U
authors.lastname: Bahner
authors.forename: Katarina
authors.initials: K
authors.lastname: Sebekova
authors.forename: Andre
authors.initials: A
authors.lastname: Klassen
authors.forename: August
authors.initials: A
authors.lastname: Heidland
mesh_terms: D000818:Animals; D050260:Carbohydrate Metabolism; D004249:DNA Damage; D042822:Genomic Instability; D017127:Glycation End Products, Advanced / Q000502:physiology*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000235:genetics* / Q000378:metabolism*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D017127:Glycation End Products, Advanced; D017382:Reactive Oxygen Species