Linked Life Data

10751631

Source:http://linkedlifedata.com/resource/pubmed/id/10751631

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2000-4-27
pubmed:abstractText
Animal cells generate hydrogen peroxide as a byproduct of energy metabolism. In the presence of reduced metals H(2)O(2) can decompose to a highly reactive hydroxyl radical that attacks essentially all organic molecules, including DNA. We wished to determine if overexpression of catalase and/or the targeting of the enzyme to the nucleus could protect cells from oxidative stress and reduce the frequency of mutation. Wild-type human catalase, which localizes to peroxisomes, and a modified construct, which targets catalase to the nucleus, were overexpressed in a murine line of embryonic carcinoma cells (P19). Both constructs enhanced the resistance of the cells to hydrogen peroxide, but sensitized them to bleomycin. Overexpression of wild-type catalase protected cells against paraquat, while nuclear targeting sensitized them to this agent. Expression of neither construct significantly altered spontaneous mutant frequencies at the endogenous murine adenosine phosphoribosyl transferase (APRT) locus; however, nuclear-targeted catalase prevented an increase in mutant frequency after H(2)O(2) treatment. These results suggest that endogenous levels of hydrogen peroxide may not generate DNA damage in vivo, or that such damage may be efficiently repaired in murine embryonic carcinoma cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0027-5107
pubmed:author
pubmed:issnType
Print
pubmed:day
3
pubmed:volume
449
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
21-31
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Overexpression of wild-type and nuclear-targeted catalase modulates resistance to oxidative stress but does not alter spontaneous mutant frequencies at APRT.
pubmed:affiliation
Department of Genetics, University of Washington, Seattle, WA, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.