Linked Life Data

17347141

Source:http://linkedlifedata.com/resource/pubmed/id/17347141

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2007-8-20
pubmed:abstractText
In an effort to define the prevalent DNA damage chemistry-associated chronic inflammation, we have quantified 12 DNA damage products in tissues from the SJL mouse model of nitric oxide (NO) overproduction. Using liquid chromatography-mass spectrometry/MS and immunoblot techniques, we analyzed spleen, liver and kidney from RcsX-stimulated and control mice for the level of the following adducts: the DNA oxidation products 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), guanidinohydantoin (Gh), oxazolone (Ox); 5-guanidino-4-nitroimidazole (NitroIm); spiroiminodihydantoin (Sp) and M(1)dG; the nitrosative deamination products 2'-deoxyxanthosine, 2'-deoxyoxanosine (dO), 2'-deoxyinosine and 2'-deoxyuridine and the lipid peroxidation-derived adducts 1,N(6)-etheno-deoxyadenosine and 1,N(2)-etheno-deoxyguanosine. The levels of dO, Gh, Ox, NitroIm and Sp were all below a detection limit of approximately 1 lesion per 10(7) bases. Whereas there were only modest increases in the spleens of RcsX-treated compared with control mice for the nucleobase deamination products (10-30%) and the DNA oxidation products 8-oxodG (10%) and M(1)dG (50%), there were large (3- to 4-fold) increases in the levels of 1,N(6)-etheno-deoxyadenosine and 1,N(2)-etheno-deoxyguanosine. Similar results were obtained with the liver and with an organ not considered to be a target for inflammation in the SJL mouse, the kidney. This latter observation suggests that oxidative and nitrosative stresses associated with inflammation can affect tissues at a distance from the activated macrophages responsible for NO overproduction during chronic inflammation. These results reveal the complexity of NO chemistry in vivo and support an important role for lipids in the pathophysiology of inflammation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0143-3334
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1807-13
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Lipid peroxidation dominates the chemistry of DNA adduct formation in a mouse model of inflammation.
pubmed:affiliation
Biological Engineering Division, Massachusetts Institute of Technology, Cambridge, MA, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural