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2-amino-alpha-carboline (AaC, 2-amino-9H-pyrido[2,3-b]indole) is a genotoxic carcinogen produced by cooking of protein-containing foods and combustion of biomaterial. Humans are chronically exposed to low levels of AaC through foods (grilled or pan-fried meats), drinking water, and smoke inhalation (cigarette/wood smoke, diesel exhaust). We report herein 17 metabolites of AaC formed in vivo in male Sprague-Dawley rats (from bile, urine, and plasma) and in situ in rat hepatocytes and human HepG2 liver tumor cells. We confirmed several expected sites of AaC metabolism, but also observed novel metabolites. The novel metabolites include extensive N-acetylated AaC conjugates, multiple N-glucuronides, and at least one additional site of aromatic ring hydroxylation. The abundance of N-acetylated metabolites is noteworthy because this metabolic pathway is generally unrecognized for HAAs. Also noteworthy are metabolites that were not detected, i.e., no direct AaC N-sulfonation to form the sulfamate. These results, combined with earlier publications on the reactive (DNA adduct forming) metabolites of AaC, indicate that both bioactivation and detoxification of AaC share the same metabolic pathways--namely, oxidation, acetylation, and sulfonation. This may be an important factor attenuating the risk of carcinogenesis from AaC exposure; increased potential for bioactivation could be balanced by increased potential for detoxification.

Metabolites of the Carcinogen 2-Amino-α-carboline Formed in Male Sprague−Dawley Rats in Vivo and in Rat Hepatocyte and Human HepG2 Cell Incubates