Abstract
Dibenzoylmethane (DBM), a curcumin-related β-diketone analogue, has been reported to exhibit a remarkable inhibitory effect on 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary tumorigenesis in Sencar mice. Investigation of the underlying mechanisms of DBM in the prevention of mammary tumorigenesis implied its role as an effector of Phase I enzymatic system. In this report, the metabolic fate of DBM by NADPH-dependent cytochrome P450 enzymes in mouse liver microsomes was demonstrated. Isolation of the major reductive metabolites of DBM (DBMH2), together with several minor metabolites identified by NMR, GC and LC-MS, explained the potential role of DBM as a modulator of the cytochrome P450 reductase that is required for the function of oxidase to metabolize DMBA. These might also contribute to the result of the inhibitory effect of DBM on DMBA-induced mouse mammary tumorigenesis.
Recommended Citation
Lin, C.-C.; Wei, G.-J.; Huang, M.-T.; and Ho, C.-T.
(2005)
"Metabolic pathway of dibenzoylmethane, a β-diketone analogue of curcumin, by NADPH-dependent cytochrome P450 enzymes in mouse liver microsomes,"
Journal of Food and Drug Analysis: Vol. 13
:
Iss.
3
, Article 3.
Available at: https://doi.org/10.38212/2224-6614.2515
