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Beta-oxidized N-nitrosoalkylcarbamates as models for DNA alkylation by N-nitrosobis(2-oxopropyl)amine in Syrian

D L Nagel1, R Lewis, M Fischer

  • 1Eppley Institute for Research in Cancer, University of Nebraska Medical Center, Omaha, Nebraska.

Insights

N-nitrosobis(2-oxopropyl)amine (NDOPA) induces pancreatic and liver tumors in hamsters. DNA analysis reveals methylation and 2-hydroxypropylation adducts, identifying key DNA damage mechanisms.

Area of Science:

  • Carcinogenesis
  • DNA adducts
  • Chemical toxicology

Background:

  • N-nitrosobis(2-oxopropyl)amine (NDOPA) is a known carcinogen that induces pancreatic duct adenocarcinomas in Syrian hamsters.
  • Previous studies indicated NDOPA causes DNA methylation in hamster pancreas and liver.

Purpose of the Study:

  • To elucidate the specific DNA adducts formed in vivo following NDOPA administration.
  • To characterize the alkylation products in hamster liver and pancreatic DNA.

Main Methods:

  • Administration of generally labeled tritiated NDOPA to Syrian hamsters.
  • Isolation and identification of DNA adducts using chromatographic and spectroscopic techniques.
  • In vitro studies using N-nitrosocarbamate models (NOPC and NHPC) with exogenous DNA and guanosine.

Main Results:

  • Tritiated NDOPA studies revealed 2-hydroxypropylation as the primary three-carbon alkylation of hamster DNA.
  • Identified N7-(2-hydroxypropyl)guanine and O6-(2-hydroxypropyl)guanine adducts in hamster liver DNA.
  • Confirmed N7-methylguanine and O6-methylguanine in DNA from both liver and pancreas.
  • In vitro models successfully predicted the formation of methylated and 2-hydroxypropylated purine adducts.

Conclusions:

  • NDOPA induces DNA damage through both methylation and 2-hydroxypropylation in hamster organs.
  • The identified adducts provide insights into the mechanism of NDOPA-induced carcinogenesis.
  • N-nitrosocarbamate models are valuable for predicting in vivo DNA adduct formation.

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