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to the rat orthologue, in N-oxidation of these HAAs (202, 207). In the case of MeIQx, oxidation of the C8-methyl group was the major pathway of transformation to form the detoxicated metabolite, 2-amino-3-methylimidazo[4,5f]quinoxaline-8-carboxylic acid (IQx-8-COOH) (223), which accounted for more than 50% of the dose excreted in the urine of subjects (196). All of the oxidation steps to form the carboxylic acid are catalyzed by P450 1A2 (224),
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a fact that underscores the prominent role of P450 1A2 in the metabolism of 8-MeIQx in humans (195). AIAs, unlike primary arylamines (225, 226), do not undergo direct metabolism by NATs to form detoxicated N-acetylated products.
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2.3.10 HEALTH RISKS OF HAAs AND UNCERTAINTIES IN ASSESSMENT Human cancer risk factor estimates for HAAs have ranged widely. An upper limit was proposed as one cancer case per 1000 individuals (227), and a lower limit as 50 cases per 106 individuals (228). The spread among the estimates can be attributed to inter-study differences in the assumptions used to calculate risk factors, including differing estimates of daily HAA intake, and the usage of TD50 values from various animal carcinogen bioassays, in which differences are seen in the HAA carcinogenic potency (229 231). As noted earlier, the actual exposure to HAAs can vary by more than 100-fold in cooked meats (2, 47, 80, 232, 233). Further complicating the extrapolation of the TD50 values, the carcinogen bioassays have used doses of HAAs at amounts exceeding the daily human exposure by 104- to 106-fold (231). Such high levels of HAA exposure may trigger metabolic pathways that preferentially lead to formation of chemically reactive metabolites normally not arising under low-dose treatments, or they may cause saturation of enzymatic detoxication systems and result in an enhanced HAA toxicity (234). In contrast to many experimental animal models, humans show large interindividual variations in the expression of cytochrome P450 enzymes and phase II enzymes that metabolize HAAs (207, 235 and references therein). The resultant differences in the expression of these enzymes may lead to different susceptibilities among individuals, which must be considered in risk assessment. Indeed, several epidemiological studies have shown a markedly increased risk of these cancers in subjects who frequently consume meats cooked welldone, and who are both rapid CYP1A2-mediated N-oxidizers and rapid acetylators (236 238): these enzymes bioactivate HAAs. There are important interspecies differences in P450 catalysis and regioselectivity of HAA oxidation; these differences affect the genotoxic potency of HAAs, and so must be taken into account when health risks are assessed (239). Diet is another obvious variable that obscures the interspecies extrapolation of toxicity data from laboratory animals to humans. In contrast to the standardized diet fed to the experimental animals, the human diet is highly diverse and complex; numerous constituents of it may enhance or diminish the genotoxic potency of HAAs. Components in grilled meats can increase the expression of P450 1A2 and the bioactivation of HAAs in humans (214). Fortunately, dietary constituents can diminish the genotoxic potential of HAAs by inhibition of P450 1A2-mediated bioactivation of HAAs (240, 241) and/or induction of the expression of GSTs (168) and UDP-glucuronosyltransferases
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(UGTs) (242), phase II enzymes involved in the detoxication of HAAs. Apiaceous vegetables, fruit juices, and beverages contain high levels of dietary components such as methoxypsoralens, apigenin, resveratrol, prenyl avonoids, and furanocoumarins, all of which are potent inhibitors of P450 1A2 activity (212, 243 246). Another uncertainty in risk assessment of HAAs is the bioavailability of HAAs in cooked foods. The bioavailability of HAAs may be reduced by dietary constituents, such as chlorophyll, which bind to HAAs (247), or by the cooked meat matrix, where increasing the doneness of the meat appears to decrease the amount of HAA accessible from the meat matrix (248). Cooked meats contain a variety of carcinogens at low concentrations, which include polycyclic aromatic hydrocarbons, N-nitroso compounds, lipid peroxides, and other pro-oxidative agents, and fungal products, in addition to HAAs. The carcinogenic potency of grilled meats and health risk may be related not only to HAAs, but also to this complex mixture of genotoxic compounds (249 251).
2.3.11 FUTURE PROSPECTS ON RESEARCH OF HAAs IN HUMAN HEALTH RISK The analysis of HAA biomarkers in humans remains a challenging analytical task, because HAAs are present at the ppb levels in the diet. However, as the sensitivity of MS instrumentation continues to improve, the establishment of LC/MS-based methods to measure biomarkers such as urinary HAA metabolites, and HAA protein and HAA DNA adducts in human populations will become more facile. Future studies will require MS analysis of biomarkers of multiple HAAs, since the extent of exposure to various HAAs can vary in the diet. Through a combination of analyses for multiple urinary metabolites, HAA protein and HAA DNA adducts, and other biomarkers of longer-term exposures, such as HAA accumulation in hair (252, 253), it may be feasible to assess more reliably the exposure to HAAs and to determine the biologically effective dose of each HAA and the resultant potential genetic damage. With the identi cation of such biomarkers, the interactive effects of genetic polymorphisms of XMEs involved in HAA metabolism (activation and detoxication) will be able to be correlated with the levels of adduction products and cancer risk in human population studies. Such analyses should clarify the role of HAAs as a critical dietary factor in the initiation of colorectal and other common human cancers.