Urinary mutagenicity on TA98 and YG1024 Salmonella typhimurium strains after a hamburger meal: influence of GSTM1 and NAT2 genotypes

Gabbani, G; Nardini, Barbara; Bordin, Anna; Pavanello, Sofia; Janni, Laura; Celotti, Lucia; Clonfero, Erminio

doi:10.1093/mutage/13.2.187

Cited by 19 publications

(14 citation statements)

References 28 publications

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“…Hamburger products have previously been reported as a major source of chemical food mutagens to consumers [38,61]. The results obtained in our study further reinforce this view, as two different lots of hamburgers examined were found to be mutagenic in all three assays in Salmonella TA 100 strain, with one of the lots (batch 2) being both directly and indirectly mutagenic in all three assays.…”

Section: Discussionsupporting

confidence: 89%

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Dietary Exposure of Nigerians to Mutagens and Estrogen-Like Chemicals

Omoruyi

Ahamioje

Pohjanvirta

2014

IJERPH

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Food and drinking water are poorly delineated sources of human exposure to chemical food mutagens and endocrine-disrupting chemicals. In this study, we investigated the presence of mutagens and chemicals exhibiting estrogenic activity in the daily diet of Nigerians, using in vitro assays. Commercially processed foods or snacks and various brands of pure water sachets were extracted by solid-phase extraction and liquid-liquid extraction, respectively. Mutagenicity was determined by the conventional Ames test and two complementary assays on two strains of Salmonella (TA 100 and TA 98), while the estrogenic activity was assessed by a yeast bioluminescent assay, using two recombinant yeast strains (Saccharomyces cerevisiae BMAEREluc/ERα and S. cerevisiae BMA64/luc). A third of the food varieties investigated (chin-chin, hamburger, suya and bean cake) were mutagenic in all three assays, either in the presence or absence of S9 mix. Of the packed water samples, five out of the sixteen investigated (31%), were found to be estrogenic, with estradiol and bisphenol A equivalents ranging from 0.79 to 44.0 ng/L and 124.2 to 1,000.8 ng/L, respectively. Hence, although the current situation in Nigeria does not appear to be substantially worse than, e.g., in Europe, regular monitoring is warranted in the future.

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Section: Discussionsupporting

confidence: 89%

“…Sodium azide is a known direct mutagen in Salmonella TA 100 [36], whereas 2-aminoantracene is metabolically activated by mono-oxygenases of the CYP1A family in rat liver [37]. Likewise, benzo[ a ]pyrene requires metabolic activation for mutagenicity [38]. …”

Section: Methodsmentioning

confidence: 99%

Dietary Exposure of Nigerians to Mutagens and Estrogen-Like Chemicals

Omoruyi

Ahamioje

Pohjanvirta

2014

IJERPH

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“…Our subjects averaged 86 kg in weight, so a typical subject had an intake of ∼344,000 rev/day from high-temperature meat; Peters et al [17] reported 253,700 rev/day in a study with a similar protocol. Extracts from fried beef and sausage were 10 times more mutagenic in YG1024 than in TA98 (Table 1), confirming a previous study [19], and was likely due to activation of HCAs by acetyltransferase in YG1024. When based instead on meat-derived mutagenicity measured in strain YG1024, our subjects had an intake of ∼3,440,000 rev/day.…”

Section: Discussionsupporting

confidence: 85%

Inhibition of Fried Meat-Induced Colorectal DNA Damage and Altered Systemic Genotoxicity in Humans by Crucifera, Chlorophyllin, and Yogurt

Shaughnessy

Gangarosa²,

Schliebe³

et al. 2011

PLoS ONE

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Dietary exposures implicated as reducing or causing risk for colorectal cancer may reduce or cause DNA damage in colon tissue; however, no one has assessed this hypothesis directly in humans. Thus, we enrolled 16 healthy volunteers in a 4-week controlled feeding study where 8 subjects were randomly assigned to dietary regimens containing meat cooked at either low (100°C) or high temperature (250°C), each for 2 weeks in a crossover design. The other 8 subjects were randomly assigned to dietary regimens containing the high-temperature meat diet alone or in combination with 3 putative mutagen inhibitors: cruciferous vegetables, yogurt, and chlorophyllin tablets, also in a crossover design. Subjects were nonsmokers, at least 18 years old, and not currently taking prescription drugs or antibiotics. We used the Salmonella assay to analyze the meat, urine, and feces for mutagenicity, and the comet assay to analyze rectal biopsies and peripheral blood lymphocytes for DNA damage. Low-temperature meat had undetectable levels of heterocyclic amines (HCAs) and was not mutagenic, whereas high-temperature meat had high HCA levels and was highly mutagenic. The high-temperature meat diet increased the mutagenicity of hydrolyzed urine and feces compared to the low-temperature meat diet. The mutagenicity of hydrolyzed urine was increased nearly twofold by the inhibitor diet, indicating that the inhibitors enhanced conjugation. Inhibitors decreased significantly the mutagenicity of un-hydrolyzed and hydrolyzed feces. The diets did not alter the levels of DNA damage in non-target white blood cells, but the inhibitor diet decreased nearly twofold the DNA damage in target colorectal cells. To our knowledge, this is the first demonstration that dietary factors can reduce DNA damage in the target tissue of fried-meat associated carcinogenesis.Trial RegistrationClinicalTrials.gov NCT00340743.

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“…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: 53%

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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Urinary mutagenicity on TA98 and YG1024 Salmonella typhimurium strains after a hamburger meal: influence of GSTM1 and NAT2 genotypes

Cited by 19 publications

References 28 publications

Dietary Exposure of Nigerians to Mutagens and Estrogen-Like Chemicals

Dietary Exposure of Nigerians to Mutagens and Estrogen-Like Chemicals

Inhibition of Fried Meat-Induced Colorectal DNA Damage and Altered Systemic Genotoxicity in Humans by Crucifera, Chlorophyllin, and Yogurt

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

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