Abstract
The mutagenicity of N-nitrosobis (2-hydroxypropyl) amine (BHP), N-nitrosobis(2-oxopropyl)amine (BOP) and N-nitroso-(2-hydroxy-propyl) (2-oxopropyl) amine (HPOP) was measured in V79 cells. Hepatocytes, used to metabolize (activate) the nitrosamines, were isolated from untreated Syrian hamsters (control) and hamsters treated with clofibrate (CLO) or dehydroepian-drosterone (DHEA) in vivo. BHP and HPOP mutagenicity increased 3- and 2-fold when hepatocytes from CLO- and DHEA-treated hamsters were used. BOP mutagenicity did not increase. 10-Undecynoic acid, a lauric acid hydroxylase inhibitor, inhibited the increase in BHP and HPOP mutagenicity by 80-90% but did not affect that of BOP. Antimycin A1, a fatty acyl coenzyme A β-oxidase inhibitor did not affect the mutagenicity of these nitrosamines. Lauric acid hydroxylase, probably omega-1 hydroxylase (cytochrome P-450 IVA2), appears to be involved in the activation of BHP and HPOP.
Original language | English (US) |
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Pages (from-to) | 177-182 |
Number of pages | 6 |
Journal | Cancer Letters |
Volume | 59 |
Issue number | 2 |
DOIs | |
State | Published - Aug 1991 |
Keywords
- cytochrome P-450
- mutagenicity
- nitrosamines
- pancreas
ASJC Scopus subject areas
- Oncology
- Cancer Research