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PMID: 6700617 Published · ppublish English Journal Article

Relationship of methyl purines produced by MNNG in adenovirus 5 DNA to viral inactivation in repair-deficient (Mer-) human tumor cell strains.

Mutation research ·Vol. 131 ·No. 2 ·1984-02-00 ·Pages 45-52

Day RS, Yarosh DB, Ziolkowski CH

Abstract

Adenovirus 5 treated with MNNG (N-methyl-N'-nitro-N-nitrosoguanidine) has greater plaque-forming ability in cell strains having the Mer+ phenotype than in strains having the Mer- phenotype. MNNG-treated Mer- strains repair the N3-methyladenine (N3MeA) but not the O6-methylguanine (O6MeG) produced in their DNA, while MNNG-treated Mer+ strains repair both of these adducts. The fate of N7-methylguanine (another DNA adduct produced by MNNG) is similar in Mer+ and Mer- strains. We show in this paper that 2.3 +/- 0.4 O6MeG and 1.4 N3MeA per adenovirus genome correlate with one lethal hit when the survival assay is done using Mer- strains as viral hosts. We suggest that O6MeG is the lesion lethal to the virus.

MeSH Terms
Adenoviruses, Human/drug effects,genetics Animals DNA/metabolism DNA Repair DNA, Viral/genetics HeLa Cells/drug effects Humans Kinetics Male Methylation Methylnitronitrosoguanidine/metabolism,toxicity Phenotype Purines/metabolism Salmon Spermatozoa Viral Plaque Assay
Chemicals
DNA, Viral Purines Methylnitronitrosoguanidine DNA
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Day R S
Yarosh D B
Ziolkowski C H
Article Info
Journal
Mutation research
Abbr.
Mutat Res
ISSN
0027-5107
Published
1984-02-00
Pages
45-52
Language
English
Region
Netherlands
NLM ID
0400763
Subset
IM
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