Formation of mutagenic activity from amino acids heated at cooking temperatures

Knize, Mark G.; Cunningham, P.L.; Avila, Julie R.; Jones, A. L.; Griffin, Edmund A.; Felton, James S.

doi:10.1016/0278-6915(84)90037-1

Cited by 24 publications

(8 citation statements)

References 18 publications

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“…None of the three HCAs was detectable in meat fried at low temperature, but all 3 were present at high levels in the meat fried at high temperature. These results are consistent with other studies [Gross and Gruter, 1992;Knize et al, 1994;Sinha et al, 1998a,b] and confirm that high temperatures are required to produce detectable levels of HCAs in cooked meat. The median intake of HCAs from fried meat was 2.2, 0.5, and 8.1 g/day for MeIQx, DiMeIQx, and PhIP, respectively.…”

Section: Intake Of Hcas Pahs and Mutagenicity Of Fried Meatsupporting

confidence: 93%

“…During the quarter century since Nagao et al [1977] discovered that the charred surface of broiled fish or beef was mutagenic, numerous studies have confirmed and extended these initial observations to many other types of foods and cooking methods [Sugimura et al, 1988;Doolittle et al, 1989;Knize et al, 1994;Felton et al, 2002]. The mutagenic activity of cooked meat has been shown to increase with different types of cooking methods [Dolara et al, 1979;Knize et al, 1985;Laser-Reutersward et al, 1987a,b;Doolittle et al, 1989], and increased cooking temperature has been shown to increase the formation of heterocyclic amines (HCAs) in meats and amino acids [Gross and Gruter, 1992;Knize et al, 1994;Sinha et al, 1998a,b].…”

Section: Introductionmentioning

confidence: 98%

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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: Intake Of Hcas Pahs and Mutagenicity Of Fried Meatsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 98%

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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“…Our early analysis (a collaboration with the group at Wageningen University, The Netherlands) of a complete human diet, with foods and amounts taken from a dietary survey and cooked under "household" conditions, also shows chromatographic types and amounts of mutagens similar to those of fried beef [Alink et al, 1988]. More recent studies show that the amounts of these compounds formed increase exponentially with temperature, and the ultimate levels attained are dependent on cooking method, cooking time, cooking temperature, and protein source [Knize et al, 1994]. In fact, the levels in some foods, such as chicken, can reach hundreds of parts per billion [Sinha et al, 1995].…”

Section: Mutagens In the Dietmentioning

confidence: 99%

Human exposure to heterocyclic amine food mutagens/carcinogens: Relevance to breast cancer

Felton

Knize

Salmon

et al. 2002

Environ and Mol Mutagen

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Heterocyclic amines produced from overcooked foods are extremely mutagenic in numerous in vitro and in vivo test systems. One of these mutagens, 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine (PhIP), induces breast tumors in rats and has been implicated in dietary epidemiology studies as raising the risk of breast cancer in humans. Efforts in our laboratory and others have centered on defining the exposure to PhIP and other dietary mutagens derived from cooked food. We accomplish this by analyzing the foods with a series of solid-phase extractions and HPLC. We have developed an LC/MS/MS method to analyze the four major human PhIP metabolites (sulfates and glucuronides) following a single meal containing 27 g of cooking-produced PhIP in 200 g of grilled meat. Although the intake of PhIP was similar for each of eight women, the total amount excreted in the urine and the metabolite profiles differed among the subjects. It appears that adsorption (digestion) from the meat matrix, other foods in the diet, and genetic differences in metabolism may contribute to the variation. The four major metabolites that can be routinely assayed in the urine are N 2 -OH-PhIP-N 2 -glucuronide, PhIP-N 2 -glucuronide, 4Ј-PhIP-glucuronide, and N 2 -OH-PhIP-N3-glucuronide. This work is suited to investigate individual exposure and risk, especially for breast cancer, from these potent dietary mutagens.

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“…Among them, temperature and cooking time are the most important because they have a profound effect on the quantities of HCAs (Knize et al, 1994a). Among them, temperature and cooking time are the most important because they have a profound effect on the quantities of HCAs (Knize et al, 1994a).…”

Section: Influence Of Time and Temperaturementioning

confidence: 99%