Effects of UV repair, error-prone repair and critical site of mutation on mutagenesis induced by N-nitromasines

M. Zielenska, Joseph Guttenplan

Research output: Contribution to journalArticle

Abstract

Many N-nitrosamines have been assayed for mutagenic activity in bacteria but few have been systematically compared in a series of strains. In this study through the use of several Salmonella tester strains, we have examined the effects of Uvr repair, error-prone repair, and the critical site for mutation (GC or AT base repair) on the mutagenic activities of a diverse group of N-nitrosamines. We have employed the histidine autotrophs, TA1975 (uvrB+), TA1535 (uvrB-) and TA100 (uvrB-/pKM101) which are hisG46 strains, sensitive mainly to G-C base damage, and TA104 (uvrB-/pKM101), a hisG428 strain, which can be reverted at the hisG428 locus by damage to A-T base-pairs, or by suppression at G-C base pairs. The N-nitrosamines studied were, N-nitroso: dimethylamine, diethylamine, dipropylamine, dibutylamine, pyrrolidine, piperidien, morpholine, methylbenzylamine, bis-(2-hydroxypropyl)amine, bis-(2-oxopropyl)amine and 3,4-dichloropyrrolidine. For all of the nitrosamines larger than diethylnitrosamine (except for methylbenzylnitrosamine) mutagenesis was greatly enhanced (3-20 ×) by the lack of uvrB activity, indicating that the DNA adducts produced by these nitrosamines can be classified as "bulky adducts". For most nitrosamines the plasmid, pKM101, enhanced mutagenesis in the hisG46 strains, several fold, suggesting that erro-prone DNA repair plays role in mutagenesis by these compounds. All of the compounds tested were more mutagenic in TA100 than TA104 except diethylnitrosamine and methylbenzylnitrosamine which were more potent in TA104. Revertants induced by all of the nitrosamines in TA100 were due predominantly to damage at G-C base pairs. Revertants induced by all the nitrosamines except diethylnitrosamine and dibutylnitrosamine resulted mainly from damage to G-C base pairs in TA104.

Original languageEnglish (US)
Pages (from-to)11-20
Number of pages10
JournalMutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
Volume180
Issue number1
DOIs
StatePublished - 1987

Fingerprint

Nitrosamines
Mutagenesis
Mutation
nitrosobenzylmethylamine
Diethylnitrosamine
Base Pairing
dibutylnitrosamine
DNA Adducts
Histidine
Salmonella
DNA Repair
Amines
Plasmids
Bacteria

Keywords

  • Critical site for mutation
  • Error-prone repair
  • N-nitrosamines
  • Salmonella tester strains
  • UVR repair

ASJC Scopus subject areas

  • Molecular Biology
  • Health, Toxicology and Mutagenesis

Cite this

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title = "Effects of UV repair, error-prone repair and critical site of mutation on mutagenesis induced by N-nitromasines",
abstract = "Many N-nitrosamines have been assayed for mutagenic activity in bacteria but few have been systematically compared in a series of strains. In this study through the use of several Salmonella tester strains, we have examined the effects of Uvr repair, error-prone repair, and the critical site for mutation (GC or AT base repair) on the mutagenic activities of a diverse group of N-nitrosamines. We have employed the histidine autotrophs, TA1975 (uvrB+), TA1535 (uvrB-) and TA100 (uvrB-/pKM101) which are hisG46 strains, sensitive mainly to G-C base damage, and TA104 (uvrB-/pKM101), a hisG428 strain, which can be reverted at the hisG428 locus by damage to A-T base-pairs, or by suppression at G-C base pairs. The N-nitrosamines studied were, N-nitroso: dimethylamine, diethylamine, dipropylamine, dibutylamine, pyrrolidine, piperidien, morpholine, methylbenzylamine, bis-(2-hydroxypropyl)amine, bis-(2-oxopropyl)amine and 3,4-dichloropyrrolidine. For all of the nitrosamines larger than diethylnitrosamine (except for methylbenzylnitrosamine) mutagenesis was greatly enhanced (3-20 ×) by the lack of uvrB activity, indicating that the DNA adducts produced by these nitrosamines can be classified as {"}bulky adducts{"}. For most nitrosamines the plasmid, pKM101, enhanced mutagenesis in the hisG46 strains, several fold, suggesting that erro-prone DNA repair plays role in mutagenesis by these compounds. All of the compounds tested were more mutagenic in TA100 than TA104 except diethylnitrosamine and methylbenzylnitrosamine which were more potent in TA104. Revertants induced by all of the nitrosamines in TA100 were due predominantly to damage at G-C base pairs. Revertants induced by all the nitrosamines except diethylnitrosamine and dibutylnitrosamine resulted mainly from damage to G-C base pairs in TA104.",
keywords = "Critical site for mutation, Error-prone repair, N-nitrosamines, Salmonella tester strains, UVR repair",
author = "M. Zielenska and Joseph Guttenplan",
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T1 - Effects of UV repair, error-prone repair and critical site of mutation on mutagenesis induced by N-nitromasines

AU - Zielenska, M.

AU - Guttenplan, Joseph

PY - 1987

Y1 - 1987

N2 - Many N-nitrosamines have been assayed for mutagenic activity in bacteria but few have been systematically compared in a series of strains. In this study through the use of several Salmonella tester strains, we have examined the effects of Uvr repair, error-prone repair, and the critical site for mutation (GC or AT base repair) on the mutagenic activities of a diverse group of N-nitrosamines. We have employed the histidine autotrophs, TA1975 (uvrB+), TA1535 (uvrB-) and TA100 (uvrB-/pKM101) which are hisG46 strains, sensitive mainly to G-C base damage, and TA104 (uvrB-/pKM101), a hisG428 strain, which can be reverted at the hisG428 locus by damage to A-T base-pairs, or by suppression at G-C base pairs. The N-nitrosamines studied were, N-nitroso: dimethylamine, diethylamine, dipropylamine, dibutylamine, pyrrolidine, piperidien, morpholine, methylbenzylamine, bis-(2-hydroxypropyl)amine, bis-(2-oxopropyl)amine and 3,4-dichloropyrrolidine. For all of the nitrosamines larger than diethylnitrosamine (except for methylbenzylnitrosamine) mutagenesis was greatly enhanced (3-20 ×) by the lack of uvrB activity, indicating that the DNA adducts produced by these nitrosamines can be classified as "bulky adducts". For most nitrosamines the plasmid, pKM101, enhanced mutagenesis in the hisG46 strains, several fold, suggesting that erro-prone DNA repair plays role in mutagenesis by these compounds. All of the compounds tested were more mutagenic in TA100 than TA104 except diethylnitrosamine and methylbenzylnitrosamine which were more potent in TA104. Revertants induced by all of the nitrosamines in TA100 were due predominantly to damage at G-C base pairs. Revertants induced by all the nitrosamines except diethylnitrosamine and dibutylnitrosamine resulted mainly from damage to G-C base pairs in TA104.

AB - Many N-nitrosamines have been assayed for mutagenic activity in bacteria but few have been systematically compared in a series of strains. In this study through the use of several Salmonella tester strains, we have examined the effects of Uvr repair, error-prone repair, and the critical site for mutation (GC or AT base repair) on the mutagenic activities of a diverse group of N-nitrosamines. We have employed the histidine autotrophs, TA1975 (uvrB+), TA1535 (uvrB-) and TA100 (uvrB-/pKM101) which are hisG46 strains, sensitive mainly to G-C base damage, and TA104 (uvrB-/pKM101), a hisG428 strain, which can be reverted at the hisG428 locus by damage to A-T base-pairs, or by suppression at G-C base pairs. The N-nitrosamines studied were, N-nitroso: dimethylamine, diethylamine, dipropylamine, dibutylamine, pyrrolidine, piperidien, morpholine, methylbenzylamine, bis-(2-hydroxypropyl)amine, bis-(2-oxopropyl)amine and 3,4-dichloropyrrolidine. For all of the nitrosamines larger than diethylnitrosamine (except for methylbenzylnitrosamine) mutagenesis was greatly enhanced (3-20 ×) by the lack of uvrB activity, indicating that the DNA adducts produced by these nitrosamines can be classified as "bulky adducts". For most nitrosamines the plasmid, pKM101, enhanced mutagenesis in the hisG46 strains, several fold, suggesting that erro-prone DNA repair plays role in mutagenesis by these compounds. All of the compounds tested were more mutagenic in TA100 than TA104 except diethylnitrosamine and methylbenzylnitrosamine which were more potent in TA104. Revertants induced by all of the nitrosamines in TA100 were due predominantly to damage at G-C base pairs. Revertants induced by all the nitrosamines except diethylnitrosamine and dibutylnitrosamine resulted mainly from damage to G-C base pairs in TA104.

KW - Critical site for mutation

KW - Error-prone repair

KW - N-nitrosamines

KW - Salmonella tester strains

KW - UVR repair

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