Abstract
Hepatocytes and pancreas duct tissues from male Syrian hamsters fed high-fat (HFD) and low-fat (LFD) diets were used to activate N-nitrosobis(2-hydroxypropyl)amine (BHP) and N-nitrosobis(2-oxopropyl)amine (BOP) In the V79 cell mutagenicity assay. V79 DNA alkylation by BHP and BOP was also measured. There was a 3.5-fold increase in BHP mutagenicity but only a 1.4-fold increase in BOP mutagenicity when hepatocytes from HFD-fed hamsters were used over the mutagenicity when hepatocytes from LFD-fed hamsters were used. When pancreas duct tissue was the activating system there was a 2-fold increase in BHP and BOP mutagenicity. O6-Methylguanine levels in V79 DNA rose 4-fold when hepatocytes from HFD-fed hamsters were used to activate BOP but they declined when BHP was the alkylating agent.

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