Urine Mutagenicity as an Indicator of Exposure to Dietary Mutagens Formed during Cooking of Foods

Baker, R.S.U.; Darnton‐Hill, Ian; Bonin, Antonio M.; Arlauskas, Andrew; Braithwaite, Candida; Wootton, M.; Truswell, A. Stewart

doi:10.2307/3430330

Cited by 3 publications

(5 citation statements)

References 3 publications

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“…The kinetics of urinary mutagenicity observed in our study are consistent with those reported in other studies, which have shown that urinary mutagenicity peaks 2-6 hr after consumption of cooked meat and declines considerably after 12-16 hr [Dolara et al, 1984;Sousa et al, 1985;Hayatsu et al, 1985;Baker et al, 1986;Ohyama et al, 1987a,b]. The significant increase in mutagenicity of hydrolyzed urine over the 7-day period might suggest an accumulation of mutagens or an enhanced production of mutagenic metabolites.…”

Section: Urinary Mutagenicity and Consumption Of Meat Cooked At Low Asupporting

confidence: 92%

“…Five years after the discovery that cooked meat was mutagenic, Baker et al [1982] demonstrated that consumption of cooked meat resulted in mutagenic urine in humans. This observation has been confirmed and extended by others [Dolara et al, 1984;Hayatsu et al, 1985;Sousa et al, 1985;Baker et al, 1986;Ohyama et al, 1987a,b;Doolittle et al, 1989;Hayatsu and Hayatsu, 1993;DeMarini et al, 1997;Gabbani et al, 1998;Johansson et al, 1998;Murray et al, 2001;Pavanello et al, 2002]. With the exception of one study involving 32 subjects [Gabbani et al, 1998] and another involving 50 [Pavanello et al, 2002], these were small studies involving 3-21 subjects that examined variables such as the type of meat or cooking method as well as the kinetics of urinary mutagenicity.…”

Section: Introductionmentioning

confidence: 55%

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Urinary mutagenesis and fried red meat intake: Influence of cooking temperature, phenotype, and genotype of metabolizing enzymes in a controlled feeding study

Peters

Sinha

Bell

et al. 2004

Environ and Mol Mutagen

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Meat cooked at high temperatures contains potential carcinogenic compounds, such as heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs). Samples from a 2-week controlled feeding study were used to examine the relationship between the intake of mutagenicity from meat fried at different temperatures and the levels of mutagenicity subsequently detected in urine, as well as the influence of the genotype of drug metabolizing enzymes on urinary mutagenicity. Sixty subjects consumed ground beef patties fried at low temperature (100 degrees C) for 1 week, followed by ground beef patties fried at high temperature (250 degrees C) the second week. Mutagenicity in the meat was assayed in Salmonella typhimurium TA98 (+S9), and urinary mutagenicity was determined using Salmonella YG1024 (+S9). Genotypes for NAT1, NAT2, GSTM1, and UGT1A1 were analyzed using blood samples from the subjects. Meat fried at 100 degrees C was not mutagenic, whereas meat fried at 250 degrees C was mutagenic (1023 rev/g). Unhydrolyzed and hydrolyzed urine samples were 22x and 131x more mutagenic, respectively, when subjects consumed red meat fried at 250 degrees C compared with red meat fried at 100 degrees C. We found that hydrolyzed urine was approximately 8x more mutagenic than unhydrolyzed urine, likely due to the deconjugation of mutagens from glucuronide. The intake of meat cooked at high temperature correlated with the mutagenicity of unhydrolyzed urine (r = 0.32, P = 0.01) and hydrolyzed urine (r = 0.34, P = 0.008). Mutagenicity in unhydrolyzed urine was not influenced by NAT1, NAT2, or GSTM1 genotypes. However, a UGT1A1*28 polymorphism that reduced UGT1A1 expression and conjugation modified the effect of intake of meat cooked at high temperature on mutagenicity of unhydrolyzed urine (P for interaction = 0.04). These mutagenicity data were also compared with previously determined levels of HCAs (measured as MeIQx, DiMeIQx, and PhIP) and polycyclic aromatic hydrocarbons (PAHs) in the meat, levels of HCAs in the urine, and CYP1A2 and NAT2 phenotypes. The levels of mutagenicity in the meat fried at low and high temperatures correlated with levels of HCAs, but not levels of PAHs, in the meat. Also, levels of mutagenicity in unhydrolyzed urine correlated with levels of MeIQx in unhydrolyzed urine (r = 0.36; P = 0.01), and the levels of mutagenicity of hydrolyzed urine correlated with levels of MeIQx (r = 0.34; P = 0.01) and PhIP (r = 0.43; P = 0.001) of hydrolyzed urine. Mutagenicity in unhydrolyzed urine was not influenced by either the CYP1A2 or NAT2 phenotype. The data from this study indicate that urinary mutagenicity correlates with mutagenic exposure from cooked meat and can potentially be used as a marker in etiological studies on cancer.

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Section: Urinary Mutagenicity and Consumption Of Meat Cooked At Low Asupporting

confidence: 92%

Section: Introductionmentioning

confidence: 55%

Urinary mutagenesis and fried red meat intake: Influence of cooking temperature, phenotype, and genotype of metabolizing enzymes in a controlled feeding study

Peters

Sinha

Bell

et al. 2004

Environ and Mol Mutagen

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“…This might affect the rectum more than the colon since the rectum is more densely vascularized and appears to have a higher basal metabolic rate than the colon (Anderson et al, 1983). Furthermore, mutagens have been reported in both feces (Hayatsu et al, 1985) and urine (Baker et al, 1986;Doolittle et al, 1989;Murray et aL., 1989) in persons who consume fried meats. The appearance of mutagens in the urine points to a systemic distribution.…”

Section: Discussionmentioning

confidence: 99%

Meat, cooking methods and colorectal cancer: A case‐referent study in Stockholm

Verdier

Hagman

Peters

et al. 1991

Intl Journal of Cancer

271

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The associations between methods of cooking meats and colorectal cancer were examined in a population-based case-referent study performed in Stockholm in 1986-1988. The study included 559 cases and 505 referents. Total meat intake, frequent consumption of brown gravy, and a preference for a heavily browned meat surface each independently increased the risk for colorectal cancer. The relative risks (RR) were higher for rectal than for colon cancer, and for boiled meat (RR colon = 1.7, RR rectum = 2.7) than for meat fried with a medium or lightly browned surface (RR colon = 0.8, RR rectum = 1.1), but the highest risks were for meat fried with a heavily browned surface (RR colon = 2.8, RR rectum = 6.0). The analyses were adjusted for year of birth, gender and fat intake. Further adjustments for total energy, dietary fiber intake, body mass and physical activity had little or no influence on the results. The findings suggest that, in addition to frequent meat intake, a heavily browned meat surface formed when frying meat at high temperatures is important in the etiology of colorectal cancer.

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“…Similarly, Sorsa et al [1985] have shown that blood carboxyhemoglobin, plasma cotinine, and urinary mutagenicity were higher in smokers than in nonsmokers, but no individual correlations were attempted, and, in fact, very high interindividual variation among the parameters tested was cited. In addition to the small numbers of participants in these studies, diet, which has been shown to influence urinary mutagenicity [Baker et al, 1982[Baker et al, , 1986Dolara et al, 1984;Sousa et al, 1985;Doolittle et al, 1989b], was…”

Section: Introductionmentioning

confidence: 96%

“…In addition to the small numbers of participants in these studies, diet, which has been shown to influence urinary mutagenicity [Baker et al, 1982[Baker et al, , 1986Dolara et al, 1984;Sousa et al, 1985;Doolittle et al, 1989b], was…”

Section: Introductionmentioning

confidence: 99%

Correlations between urinary nicotine or cotinine and urinary mutagenicity in smokers on controlled diets

Howard

Riccio

et al. 1991

Environ and Mol Mutagen

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Cigarette smokers have been reported to void urine that is more mutagenic, as measured in the Salmonella/microsome assay, than urine voided by nonsmokers. Several previous studies have attempted to correlate indices of tobacco smoke exposure (e.g. nicotine, cotinine, tar intake) with urinary mutagenicity, with conflicting results. These studies generally involved small numbers of smokers and did not carefully control diet, which is known to affect urinary mutagenicity markedly. Our objective was to conduct a controlled study to determine clearly if there were a correlation between urinary nicotine, cotinine, or nicotine + cotinine and urinary mutagenicity and to determine if nicotine or its major metabolite plays a role in the mutagenicity of urine from cigarette smokers. We used a large number of smokers (31), each of whom smoked both a tobacco-burning cigarette and a tobacco-heating cigarette on consecutive weeks, and we prepared and served identical diets to all subjects. Nicotine and cotinine concentrations were determined in small aliquots from urine samples collected over 24 hr, and the remaining urine sample was extracted and concentrated on XAD-2 resin for mutagenicity assays in the Salmonella/microsome test. Nicotine, cotinine, and nicotine + cotinine were statistically correlated with mutagenicity of urine from smokers of the tobacco-burning cigarette, but there was no correlation between nicotine, cotinine, or nicotine + cotinine and mutagenicity of urine from smokers of the tobacco-heating cigarettes. Thus, although urinary nicotine and cotinine concentrations correlate with urinary mutagenicity in smokers of tobacco-burning cigarettes, the present results indicate that nicotine and its metabolite are not responsible for the mutagenicity of smokers' urine.

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Urine Mutagenicity as an Indicator of Exposure to Dietary Mutagens Formed during Cooking of Foods

Cited by 3 publications

References 3 publications

Urinary mutagenesis and fried red meat intake: Influence of cooking temperature, phenotype, and genotype of metabolizing enzymes in a controlled feeding study

Urinary mutagenesis and fried red meat intake: Influence of cooking temperature, phenotype, and genotype of metabolizing enzymes in a controlled feeding study

Meat, cooking methods and colorectal cancer: A case‐referent study in Stockholm

Correlations between urinary nicotine or cotinine and urinary mutagenicity in smokers on controlled diets

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