Polycyclic aromatic hydrocarbon (PAH) is a family of carcinogens which require metabolic activation to exert their carcinogenic properties. Benzo[a]pyrene (B[a]P) is one of the most carcinogenic family members of PAH and is a known component of cigarette smoke. Three major metabolic pathways for B[a]P were proposed, which include P450 catalyzed diol epoxide pathway, peroxidase catalyzed radical cation pathway and aldoketo reductase (AKR) catalyzed o-quinone pathway. It is known that cigarette smoke can induce P450 and AKR gene expression levels in lung cells and levels of PAH exposure has direct connections with human lung cancer occurrence. We studied B[a]P metabolism in human bronchia epithelium cell (HBEC-kt) by a stable isotope dilution APCI LC-MS/MS method. We also investigated the contributions of P450 and AKR inducers in B[a]P metabolism to understand the relationship between metabolite level and metabolizing enzyme gene expression level in this cell model. [Supported by 1P30-ES013508 and 1R01-ES-15857 to TMP]

Relationship between metabolizing enzyme gene expression and metabolite profiling of B[<i>a</i>]P metabolism in human bronchia epithelium cells

244th National Meeting (2012)

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Relationship between metabolizing enzyme gene expression and metabolite profiling of B[a]P metabolism in human bronchia epithelium cells