Mutation of V79 cells by N-dialkylnitrosamines after activation by hamster pancreas duct cells

Terence Lawson, Carol Kolar

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Pancreas duct epithelial cells (DEC), isolated from hamsters and cultured for up to 25 days, were able to metabolize N-nitrosobis(2-oxopropyl)amine (BOP) to species that were mutagenic in V79 cells. There was no decline in the nitrosamine-activating ability of DEC over the period of observation (25 d). DEC activated N-nitrosobis(2-hydroxypropyl)amine (BHP), N-nitrosodiethylamine (DEN), N-nitrosodimethylamine (DMN) and N-nitrosomethyl(2-oxopropyl)amine (MOP) and BOP in the same assay, although the mutation frequencies for BHP, DEN and DMN were barely different from that for the controls (4 ± 1 mutants/106 cells). The mutation frequencies for a dose of 0.1 mM were BHP, 2 ± 1; BOP, 113 ± 7; DEN, 8 ± 1; DMN, 5 ± 2; and MOP, 18 ± 3 (mutants/106 cells; means ± SE). When hepatocytes were used the mutation frequencies were BHP, 3 ± 1; BOP, 60 ± 3; DEN, 8 ± 2; DMN, 8 ± 2; and MOP, 121 ± 10. BOP was toxic to the DEC at doses above 0.1 mM. Experiments in which co-factors were omitted from the medium suggested that an isoform(s) of the cytochrome P-450 IIIA family was involved, directly or indirectly, in BOP activation.

Original languageEnglish (US)
Pages (from-to)139-144
Number of pages6
JournalMutation Research/Environmental Mutagenesis and Related Subjects
Volume272
Issue number2
DOIs
StatePublished - Oct 1992

Fingerprint

Cricetinae
Ducts
Pancreas
Mutation Rate
Epithelial Cells
Chemical activation
Mutation
diisopropanolnitrosamine
nitrosobis(2-oxopropyl)amine
Methoxsalen
Dimethylnitrosamine
Diethylnitrosamine
Nitrosamines
Poisons
Cytochrome P-450 Enzyme System
Amines
Hepatocytes
Assays
Protein Isoforms
Observation

Keywords

  • Duct epithelium
  • Hamster pancreas duct cells
  • Nitrosamine
  • Pancreas
  • V79 cells

ASJC Scopus subject areas

  • Toxicology
  • Genetics

Cite this

Mutation of V79 cells by N-dialkylnitrosamines after activation by hamster pancreas duct cells. / Lawson, Terence; Kolar, Carol.

In: Mutation Research/Environmental Mutagenesis and Related Subjects, Vol. 272, No. 2, 10.1992, p. 139-144.

Research output: Contribution to journalArticle

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abstract = "Pancreas duct epithelial cells (DEC), isolated from hamsters and cultured for up to 25 days, were able to metabolize N-nitrosobis(2-oxopropyl)amine (BOP) to species that were mutagenic in V79 cells. There was no decline in the nitrosamine-activating ability of DEC over the period of observation (25 d). DEC activated N-nitrosobis(2-hydroxypropyl)amine (BHP), N-nitrosodiethylamine (DEN), N-nitrosodimethylamine (DMN) and N-nitrosomethyl(2-oxopropyl)amine (MOP) and BOP in the same assay, although the mutation frequencies for BHP, DEN and DMN were barely different from that for the controls (4 ± 1 mutants/106 cells). The mutation frequencies for a dose of 0.1 mM were BHP, 2 ± 1; BOP, 113 ± 7; DEN, 8 ± 1; DMN, 5 ± 2; and MOP, 18 ± 3 (mutants/106 cells; means ± SE). When hepatocytes were used the mutation frequencies were BHP, 3 ± 1; BOP, 60 ± 3; DEN, 8 ± 2; DMN, 8 ± 2; and MOP, 121 ± 10. BOP was toxic to the DEC at doses above 0.1 mM. Experiments in which co-factors were omitted from the medium suggested that an isoform(s) of the cytochrome P-450 IIIA family was involved, directly or indirectly, in BOP activation.",
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AB - Pancreas duct epithelial cells (DEC), isolated from hamsters and cultured for up to 25 days, were able to metabolize N-nitrosobis(2-oxopropyl)amine (BOP) to species that were mutagenic in V79 cells. There was no decline in the nitrosamine-activating ability of DEC over the period of observation (25 d). DEC activated N-nitrosobis(2-hydroxypropyl)amine (BHP), N-nitrosodiethylamine (DEN), N-nitrosodimethylamine (DMN) and N-nitrosomethyl(2-oxopropyl)amine (MOP) and BOP in the same assay, although the mutation frequencies for BHP, DEN and DMN were barely different from that for the controls (4 ± 1 mutants/106 cells). The mutation frequencies for a dose of 0.1 mM were BHP, 2 ± 1; BOP, 113 ± 7; DEN, 8 ± 1; DMN, 5 ± 2; and MOP, 18 ± 3 (mutants/106 cells; means ± SE). When hepatocytes were used the mutation frequencies were BHP, 3 ± 1; BOP, 60 ± 3; DEN, 8 ± 2; DMN, 8 ± 2; and MOP, 121 ± 10. BOP was toxic to the DEC at doses above 0.1 mM. Experiments in which co-factors were omitted from the medium suggested that an isoform(s) of the cytochrome P-450 IIIA family was involved, directly or indirectly, in BOP activation.

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