Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2003-4-17
pubmed:abstractText
Reactive oxygen species are formed as by-products of mitochondrial aerobic respiration, as induced products upon exposure to certain environmental/exogenous agents (e.g. ionizing radiation), or as intended products during the immune response against invading foreign microbes. Although serving as essential signaling molecules in certain biological processes (e.g. during gene activation responses), these chemicals, particularly during oxidative stress when at excessive concentrations, can react with cellular components, most notably DNA, and in this capacity, promote mutagenesis or cell death, and in turn, human disease. We review here several of the common oxidative DNA damages as well as the DNA repair mechanisms related to maintaining genome integrity, and thus, preventing cancer formation and age-related disease. We focus mainly on participants of the base excision repair (BER) pathway. In brief, the steps of BER include: (a) excision of the damaged base, (b) incision of the DNA backbone at the apurinic/apyrimidinic (AP) site product, (c) removal of the AP terminal fragment, (d) gap-filling synthesis, and (e) ligation of the final nick.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1093-4715
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
d963-81
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Repair mechanisms for oxidative DNA damage.
pubmed:affiliation
Laboratory of Molecular Gerontology, GRC, National Institute on Aging, IRP, NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224-6825, USA. wilsonda@grc.nia.nih.gov
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review