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Title: The role of 8-oxoguanine DNA glycosylase-1 in inflammation.

Authors: Ba, Xueqing; Aguilera-Aguirre, Leopoldo; Rashid, Qura Tul Ain Nmi; Bacsi, Attila; Radak, Zsolt; Sur, Sanjiv; Hosoki, Koa; Hegde, Muralidhar L; Boldogh, Istvan

Published In Int J Mol Sci, (2014 Sep 23)

Abstract: Many, if not all, environmental pollutants/chemicals and infectious agents increase intracellular levels of reactive oxygen species (ROS) at the site of exposure. ROS not only function as intracellular signaling entities, but also induce damage to cellular molecules including DNA. Among the several dozen ROS-induced DNA base lesions generated in the genome, 8-oxo-7,8-dihydroguanine (8-oxoG) is one of the most abundant because of guanine's lowest redox potential among DNA bases. In mammalian cells, 8-oxoG is repaired by the 8-oxoguanine DNA glycosylase-1 (OGG1)-initiated DNA base excision repair pathway (OGG1-BER). Accumulation of 8-oxoG in DNA has traditionally been associated with mutagenesis, as well as various human diseases and aging processes, while the free 8-oxoG base in body fluids is one of the best biomarkers of ongoing pathophysiological processes. In this review, we discuss the biological significance of the 8-oxoG base and particularly the role of OGG1-BER in the activation of small GTPases and changes in gene expression, including those that regulate pro-inflammatory chemokines/cytokines and cause inflammation.

PubMed ID: 25250913 Exiting the NIEHS site

MeSH Terms: Animals; Body Fluids/chemistry; Chronic Disease; Cytokines/biosynthesis; Cytokines/genetics; DNA Damage; DNA Glycosylases/deficiency; DNA Glycosylases/genetics; DNA Glycosylases/physiology*; DNA Repair/physiology*; Environmental Pollutants/toxicity; Enzyme Activation; Epithelial Cells/enzymology; Epithelial Cells/pathology; GTP Phosphohydrolases/metabolism; Gene Expression Regulation; Guanine/analogs & derivatives*; Guanine/metabolism; Humans; Inflammation/enzymology*; Inflammation/genetics; Inflammation/pathology; Lung Diseases/enzymology; Lung Diseases/etiology; Lung Diseases/genetics; Mice; Mice, Inbred BALB C; Mice, Knockout; Mutagenesis; Oxidative Stress; RNA Interference; Reactive Oxygen Species/metabolism; Respiratory System/enzymology; Respiratory System/pathology

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