values were calculated to be 0.21 μM (NAT), 0.23 μM (NAB) and 8.51 μM (nicotine) for OPB formation; 0.71 μM (NAT), 0.87 μM (NAB) and 25.01 μM (nicotine) for HPB formation and 0.36 μM (NAT), 0.50 μM (NAB) and 6.57 μM (nicotine) for OPBA formation, respectively. In addition, the study of the transformation of the three metabolites revealed OPB was not only an end product but also an intermediate product of the CYP2A13-catalyzed NNK metabolism. These results suggest that structurally similar tobacco constituents with weak or no carcinogenicity influence the metabolic activation of NNK, which interferes with its carcinogenicity to some extent.
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Liu et al. (2016) studied this question.
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