rdf:type |
|
lifeskim:mentions |
umls-concept:C0004135,
umls-concept:C0007600,
umls-concept:C0022702,
umls-concept:C0036667,
umls-concept:C0043240,
umls-concept:C0069225,
umls-concept:C0086418,
umls-concept:C0178539,
umls-concept:C0205307,
umls-concept:C0312418,
umls-concept:C0374711,
umls-concept:C1516240,
umls-concept:C1705181,
umls-concept:C1707520,
umls-concept:C2917430
|
pubmed:issue |
12 Pt 1
|
pubmed:dateCreated |
1982-2-25
|
pubmed:abstractText |
Human lymphoblastoid cell lines from normal individuals and from patients with ataxia telangiectasia were either proficient or deficient in their ability to repair the mutagenic DNA adduct O6-methylguanine that is induced by methylating carcinogens. There was no relationship between the capacity to repair O6-methylguanine and the ataxia telangiectasia phenotype. Time-course studies done following a short pulse (2 min) of alkylation with 0.5 microgram of N-[3H]methyl-N'-nitro-N-nitrosguanidine per ml revealed that the repair of O6-methylguanine in human lymphoblastoid lines proficient in this ability is a rapid process, which proceeds with a half-life of 10 to 15 min. Lymphoblastoid lines with deficient capacity to repair this DNA adduct were hypersensitive to the cytotoxic effect of the methylating carcinogens N-methyl-N'-nitro-N-nitrosoguanidine, N-methyl-N-nitrosourea, and methyl methanesulfonate, and this hypersensitivity was correlated with the relative amount of O6-methylguanine induced by each of the three chemicals. This was taken as an indication of the lethality of unrepaired O6-methylgluanine. The extent of DNA repair synthesis induced by the three carcinogens was the same in cell lines proficient and deficient in O6-methylguanine repair, indicating no major deficiency in an excision repair pathway in the hypersensitive cell lines.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Dec
|
pubmed:issn |
0008-5472
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
41
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
5114-20
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:7307010-Adolescent,
pubmed-meshheading:7307010-Adult,
pubmed-meshheading:7307010-Alkylating Agents,
pubmed-meshheading:7307010-Ataxia Telangiectasia,
pubmed-meshheading:7307010-Cell Division,
pubmed-meshheading:7307010-Cells, Cultured,
pubmed-meshheading:7307010-Child,
pubmed-meshheading:7307010-DNA,
pubmed-meshheading:7307010-DNA Repair,
pubmed-meshheading:7307010-Female,
pubmed-meshheading:7307010-Guanine,
pubmed-meshheading:7307010-Humans,
pubmed-meshheading:7307010-Infant, Newborn,
pubmed-meshheading:7307010-Kinetics,
pubmed-meshheading:7307010-Male,
pubmed-meshheading:7307010-Methyl Methanesulfonate,
pubmed-meshheading:7307010-Methylation,
pubmed-meshheading:7307010-Methylnitronitrosoguanidine,
pubmed-meshheading:7307010-Methylnitrosourea
|
pubmed:year |
1981
|
pubmed:articleTitle |
Kinetics of O6-methylguanine repair in human normal and ataxia telangiectasia cell lines and correlation of repair capacity with cellular sensitivity to methylating agents.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.
|