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PubMed1980

Clinical aspects of acute pelvic inflammatory disease: Cook County Hospital.

We reviewed Cook County Hospital records of 134 consecutive patients hospitalized for acute pelvic inflammatory disease unrelated to intrauterine devices, delivery, or pelvic surgery. Nearly half our patients had peritonitis or a pelvic mass and most were young or nulliparous. Neisseria gonorrhoeae was recovered from the endocervices of 41 (34%) of 120 patients and was more common among younger patients. Most patients responded to antibiotic therapy; consequently, we recommend antibiotic treatment for acute PID unless surgical emergencies cannot be excluded or patients do not improve with antibiotic therapy alone.

Adult↗

PubMed1993

Cook obstetrics and gynecology catheter multicenter chorionic villus sampling trial: comparison of birth defects with expected rates.

OBJECTIVE: The null hypothesis was that offspring of women undergoing first-trimester chorionic villus sampling do not experience a rate of birth defects exceeding background rates. STUDY DESIGN: Follow-up information regarding major malformations was prospectively sought on offspring of 4105 women undergoing first-trimester chorionic villus sampling from nine centers participating in a collaborative study with the Cook obstetrics and gynecology catheter. These data were compared with data from the Collaborative Perinatal Project and other registries. RESULTS: A total of 84 offspring with major malformations was identified (2.36%). Compared with background rates, there was no increase in the incidence of total malformations or specific malformations (including limb reduction defects) in the subjects. One institution experienced all three limb reduction defects in this series; the probability of this occurring by chance alone is < 1%. CONCLUSION: Chorionic villus sampling was not found to result in an increase in major birth defects or in specific categories of birth defects in this series.

Catheterization↗

PubMed1984

The establishment of the bacterium Streptococcus mutans in dental plaque and the induction of caries in macaque monkeys (Macaca fascicularis) fed a diet containing cooked-wheat flour.

A diet containing 50.7 per cent cooked wheat flour (78 per cent starches and dextrin) was fed to 82 monkeys from weaning for up to 407 days. Streptococcus mutans became established naturally and remained at a high level (25-40 per cent of the total anaerobic colony count) in the dental plaque of the majority of animals but in only 2 were carious lesions detected. The predominant Strep. mutans serotypes isolated from plaque were c, e and h, which produced acid when incubated with the diet in vitro. Twenty-five monkeys were switched to a cariogenic high sucrose diet, and 6 months later 72 per cent of them had carious lesions (mean +/- SD = 6.5 +/- 6.6 carious lesions per monkey). The failure of the starch diet to promote tooth decay in monkeys supports the general conclusion that starch and starch products are virtually non-cariogenic for man.

Animals↗

PubMed1985

Comparative mutagenic efficiencies of the DNA adducts from the cooked-food-related mutagens Trp-P-2 and IQ in CHO cells.

The relationship between DNA-adduct formation and mutagenicity of two heterocyclic aromatic amines associated with cooked foods was determined in a CHO cell strain lacking nucleotide excision repair. Cells were exposed to tritiated IQ (2-amino-3-methylimidazo[4,5-f]quinoline) or Trp-P-2 (3-amino-1-methyl-5H-pyrido[4,3-b]indole) supplemented with hamster S9 microsomal fraction for metabolic activation. DNA from nuclei was isolated by DNAase-mediated elution from polycarbonate filters after RNAase and proteinase treatment. The presumed metabolites of both compounds bound to DNA in a dose-dependent fashion. Although the dose required to produce 50% cell killing was 15 times higher for IQ than Trp-P-2, the amount of radioactive material bound to DNA at that dose was about 10-fold lower with IQ. When mutations at the hprt and aprt loci were compared with the estimated levels of adducts, the calculated mutagenic efficiency of the adducts was about 4 mutations per 1000 adducts for both compounds, assuming a target sequence of 1000 base pairs for either locus. We conclude that IQ is acting as a weak mutagen in this system because its extracellular metabolites either do not reach or do not react efficiently with the DNA of the CHO cells.

Animals↗

PubMed1986

Effects of plant-derived flavonoids and polyphenolic acids on the activity of mutagens from cooked food.

The ability of 3 plant flavonoids (morin, myricetin and quercetin) and 4 polyphenolic acids (caffeic acid, chlorogenic acid, ellagic acid and ferulic acid) to inhibit the genotoxic effects of a number of cooked-food mutagens (IQ, MeIQ, MeIQx, Trp-P-1 and Trp-P-2), was investigated in a bacterial mutation assay using Salmonella typhimurium TA98 as indicator and hepatic S9 mixes from either SWR mice or Syrian hamsters as metabolic activating systems. Although the polyphenolic acids failed to have an effect, the flavonoids generally inhibited IQ, MeIQ, MeIQx and Trp-P-1 induced mutagenesis in a dose-dependent manner, irrespective of the source of S9. This was not the case with Trp-P-2 where the flavonoids were only observed to inhibit when SWR mouse S9 but not Syrian hamster S9 was used. Of the 3 compounds, myricetin and quercetin were superior to morin in their inhibitory capacity.

Animals↗

PubMed1988

Presence of nitrosable mutagen precursors in cooked meat and fish.

Broiled chicken, pork, mutton, beef and sun-dried sardine were found to yield direct-acting mutagenicity after nitrite treatment. When 50% methanol extracts of cooked foods were treated with 50 mM nitrite at pH 3 for 1 h at 37 degrees C, they induced 3800-17,900 revertants of Salmonella typhimurium TA100 and 15,000-43,600 revertants of TA98 per g. In contrast, raw meat and uncooked sun-dried sardine showed little or no mutagenicity after nitrite treatment. Treatment of broiled chicken with 0.5-3 mM nitrite, which is a physiologically feasible concentration in the human stomach under some conditions, induced direct-acting mutagenicity. When broiled chicken was treated with 1 mM nitrite at pH 3 for 1 h at 37 degrees C, its mutagenicities on TA100 and TA98 without S9 mix were 7100 and 5400 revertants/g, respectively.

Animals↗

PubMed1992

Quantitative correlation of mutagenic and carcinogenic potencies for heterocyclic amines from cooked foods and additional aromatic amines.

Aromatic amines have long been recognized as animal and human carcinogens. Recently heterocyclic aromatic amines (thermic amines) have been found in small amounts in cooked foods, primarily meats, and have proven to be potent mutagens and rodent carcinogens. Availability of quantitative databases for mutagenic potency in Salmonella and for carcinogenic potency in rodents has made possible a study of ten heterocyclic thermic amines and 24 aromatic amines. Potencies on mutagenic and carcinogenic scales were significantly correlated. By multiple linear regression analysis and multivariate analysis of variance, two descriptive structural factors were found to modulate the two modes of biological response. These factors were number of rings and methyl substitution at carbon atoms. The quantitative correlation between mutagenic and carcinogenic potencies and the modulating structural factors suggest a significant similarity of molecular mechanisms and support the utility of the short-term bacterial assay in evaluating hazard levels.

Amines↗

PubMed1988

L-tryptophan inhibits formation of mutagens during cooking of meat and in laboratory models.

The formation of mutagens and carcinogens of the 2-amino-3-methylimidazo[4,5-f]quinoline and -quinoxaline type, formed during the frying or broiling of meats and in liquid-reflux laboratory models, was inhibited by L-tryptophan in a dose-dependent fashion. Addition of 75 mg (1.04 mg/cm2 surface area) of L-tryptophan per side in a sauce to ground beef patties prior to cooking significantly blocked the formation of mutagens observed in control patties treated identically with sauce but without L-tryptophan. The sauce itself did not have a significant inhibitory effect. When a mixture of 35 mM glucose, 70 mM glycine, and 70 mM creatinine in diethylene glycol-water (95:5) was heated in a liquid-reflux model for 2 h at 150 degrees C, the addition of 1.75-105 mM L-tryptophan gave a dose-related inhibition of mutagen formation, that reached 100% inhibition with 105 mM L-tryptophan.

Animals↗

PubMedDate not supplied

In vivo cytogenetic effects of the cooked-food-related mutagens Trp-P-2 and IQ in mouse bone marrow.

Sister-chromatid exchange and chromosomal aberrations were measured in vivo in mouse bone marrow following intraperitoneal injection of the cooked food mutagens, Trp-P-2 and IQ. Trp-P-2 produced a significant positive dose response for both endpoints while IQ produced only a weak but significant sister-chromatid exchange response. The relative potency of these two chemicals is similar to that seen in mammalian cells in vitro but opposite to their potency in Salmonella.

Animals↗

PubMedDate not supplied

Formation of a mutagen, 2-amino-1-methyl-6-phenylimidazo[4,5-b]-pyridine (PhIP) in cooked beef, by heating a mixture containing creatinine, phenylalanine and glucose.

When a mixture of creatinine, phenylalanine and glucose in diethylene glycol-water solution was heated for 2 h at 128 degrees C, a mutagen, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), was found to be produced, identified by high-performance liquid chromatography, and UV-visible and mass spectrometries. The yield of PhIP was 3.6 nmoles/mmole original creatinine. PhIP was originally isolated from cooked beef, and this study shows creatinine, phenylalanine and glucose to be the probable precursors of PhIP in beef.

Animals↗

PubMed1989

Shelf-life of vacuum-packed cooked ring sausages at different chill temperatures.

Microbiological and sensory changes in 313 vacuum-packed cooked ring sausages from 28 different production runs and stored at 2, 4, 8 or 12 degrees C were monitored as a function of time. The sensory scores started to decrease at a level of approx. 10(7) lactobacilli/g. The judges began considering the samples unfit for human consumption when the lactobacilli counts were between 10(7) and 10(8) cfu/g; above a level of 10(8) cfu/g most of the samples were deemed unfit. At 2 degrees C, however, spoilage did not always seem to be microbiological, and four out of six different production runs were deemed unfit without any marked increase in microbial counts. In such cases, the judges described the sensory defects as a 'musty' rather than a sour aroma and taste. The sausages were deemed unfit when the lactobacilli were in a stationary growth phase which was considerably later than the point when the bacterial counts exceeded 10(7) cfu/g. The mean length of this delay was 30, 19, 16 and 7 days at 2, 4, 8 and 12 degrees C, respectively. The average shelf-lives were 55, 43, 29 and 17 days at 2, 4, 8 and 12 degrees C, respectively. The dependence of shelf-life on temperature can be formulated as follows: Shelf-life = 10(1.835 - 0.048 X temperature) The maximal shelf-life of this product, including nonmicrobiological spoilage, is assessed as approx. 10-11 weeks. A lactobacilli count greater than 10(7) cfu/g indicates that either the spoilage process has started or the product is already spoiled. When the lactobacilli count exceeds 10(8) cfu/g it is highly probable that the sausage sample is unacceptable.

Cold Temperature↗

PubMed1990

Lactic acid and pH as indicators of spoilage for vacuum-packed cooked ring sausages.

Lactic acid production and pH changes of 206 vacuum-packed cooked ring sausages stored at 2, 4 and 12 degrees C from 21 different production runs were monitored as a function of time and of microbial growth. The total lactic acid concentrations and pH values were first at a constant level, starting to increase sharply after the lactobacilli count reached about 5 x 10(7) or 6 x 10(7) cfu/g, respectively. The lactic acid and pH changes as a function of the lactobacilli count were similar at 4 and 12 degrees C. The sharp increase at high lactobacilli counts was observed in both L-lactic acid and D-lactic acid. The variation was lesser and the increase greater in D-lactic acid formation than in L-lactic acid. Above a level of 3-4 mg lactic acid/g most of the samples were deemed unfit. The pH started to decrease from a level of approx. 6.3; below 5.8-5.9 the samples were deemed unfit. The lowest pH value observed was 4.58. Both a high lactic acid content and a low pH indicated that the sausage was spoiled. These changes, however, took place at later stages of storage, and do not give information about the early phase of spoilage.

Animals↗

PubMed1986

Induction of unscheduled DNA synthesis in rat and hamster hepatocytes by cooked food mutagens.

The genotoxicity of the cooked-food mutagens 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) and 3-amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2) was studied by monitoring the induction of DNA repair (unscheduled DNA synthesis; UDS) in primary cultures of rodent hepatocytes. The hepatocytes were derived from male Sprague-Dawley rats or Syrian hamsters by collagenase perfusion and the cells were cultured for 4 hr before being exposed to various concentrations of the mutagens. DNA repair was determined by measuring incorporation of [3H]thymidine into extracted DNA over 17 hr using beta-scintillation counting. Dose-related increases in UDS were clearly seen in hamster hepatocytes treated with MeIQ, IQ and the positive control 2-acetylaminofluorene (AAF), and a weak response was induced by MeIQx and Trp-P-1. In the rat hepatocytes only MeIQ and AAF gave clear positive responses. Furthermore it was noted that all the mutagens displayed a more pronounced UDS response in hamster hepatocytes than in rat cells. Studies of the activation of MeIQ by hepatocytes to a bacterial mutagen suggest that this difference is probably a consequence of the greater capacity of hamster cells to activate the mutagens to genotoxic metabolites.

Animals↗

PubMed1995

Genetically modified Chinese hamster ovary (CHO) cells for studying the genotoxicity of heterocyclic amines from cooked foods.

We have developed metabolically competent Chinese hamster ovary (CHO) cells to evaluate the genotoxicity associated with heterocyclic amines, such as those that are present in cooked foods. Into repair-deficient UV5 cells we introduced cDNAs for expressing cytochrome P450IA2 and acetyltransferases. We then genetically reverted these transformed lines to obtain matched metabolically competent repair-deficient/proficient lines. For a high mutagenic response, we find a requirement for acetyltransferase with 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) but not with 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). This system allows for both quantifying mutagenesis and analyzing the mutational spectra produced by heterocyclic amines.

Animals↗

PubMed1987

Effect of water-soluble fraction of Cook Inlet crude oil on swimming performance and plasma cortisol in juvenile coho salmon (Oncorhynchus kisutch).

Swimming performance of juvenile coho salmon decreased and plasma cortisol increased, following 48-hr exposure to the water-soluble fraction (WSF) of Cook Inlet crude oil at 75% of the LC50. Exposure to 25 and 50% of the LC50 did not significantly reduce swimming performance. Plasma cortisol concentrations were highest in fish exposed to both the combined stress of WSF exposure and of forced swimming in a stamina tunnel.

Animals↗

PubMed2006

Cytochrome P450 expression and metabolic activation of cooked food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in MCF10A breast epithelial cells.

The cytochrome P450 expression profile was determined in the MCF10A human breast epithelial cell line, as was the ability of this cell line to catalyze the bioactivation of the cooked food mutagen, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). Using non-quantitative reverse transcription-polymerase chain reaction (RT-PCR), transcripts for CYP1B1, CYP2J2, CYP2R1, CYP2U1, CYP2W1, CYP4B1, CYP4F, CYP4V2, CYP4X1 and CYP4Z1 were detected in both sub-confluent and confluent MCF10A cells. By contrast, CYP1A2 mRNA was detected only in confluent MCF10A cells, while CYP1A1, CYP2S1 and CYP2F1 were detected predominantly or exclusively in sub-confluent cultures. 2,3,7,8-Tetrachlorodibenzo-p-dioxin treatment of confluent MCF10A cells markedly induced microsomal ethoxyresorufin O-deethylase activity and CYP1A1, CYP1A2 and CYP1B1 mRNA levels, as determined by real-time RT-PCR, while treatment with 10(-4)M PhIP had little effect on these P450 transcript levels. Treatment of confluent MCF10A cells with PhIP (10(-4)M) for 24, 48 or 72 h produced time-dependent increases in the amounts of DNA adducts, as measured by (32)P-post-labeling. These results indicate that multiple P450s, including those known to catalyze PhIP N-oxidation, are expressed in MCF10A cells, and that this non-neoplastic human breast epithelial cell line contains sufficient enzymatic machinery to support PhIP bioactivation and generate DNA damage.

Aryl Hydrocarbon Hydroxylases↗

PubMed2006

Predictive model for growth of Clostridium perfringens in cooked cured pork.

Mathematical models have been developed and used for predicting growth of foodborne pathogens in various food matrices. However, these early models either used microbiological media or other model systems to develop the predictive models. Some of these models have been shown to be inaccurate for applications in meat and specific food matrices, especially under dynamic conditions, such as constantly changing temperatures that are encountered during food processing. The objective of this investigation was to develop a model for predicting growth of Clostridium perfringens from spore inocula in cured pork ham. Isothermal growth of C. perfringens at various temperatures from 10 to 48.9 degrees C were evaluated using a methodology that employed a numerical technique to solve a set of differential equations. The estimated theoretical minimum and maximum growth temperatures of C. perfringens in cooked cured pork were 13.5 and 50.6 degrees C, respectively. The kinetic and growth parameters obtained from this study can be used in evaluating growth of C. perfringens from spore populations during dynamically changing temperature conditions such as those encountered in meat processing. Further, this model can be successfully used to design microbiologically "safe" cooling regimes for cured pork hams and similar products.

Animals↗

PubMed2005

The effect of UDP-glucuronosyltransferase 1A1 expression on the mutagenicity and metabolism of the cooked-food carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine in CHO cells.

UDP-glucuronosyltransferase proteins (UGT) catalyze the glucuronidation of both endogenous and xenobiotic compounds. In previous studies, UGT1A1 has been implicated in the detoxification of certain food-borne carcinogenic-heterocyclic amines. To determine the importance of UDP-glucuronosyltransferase 1A1 (UGT1A1) in the biotransformation of the cooked-food carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), genetically modified CHO cells that are nucleotide excision repair-deficient, and express cytochrome P4501A2 (UV5P3 cell line) were transfected with a cDNA plasmid of human UGT1A1 to establish the UDP-glucuronosyltransferase 1A1 expressing 5P3hUGT1A1 cell line. Expression of the UGT1A1 gene was verified by screening neo gene expressing clonal isolates (G-418 resistant) for their sensitivity to cell killing from PhIP exposure. Five of 11 clones were chosen for further analysis due to their resistance to cell killing. Western blot analysis was used to confirm the presence of the UGT1A1 and CYP1A2 proteins. All five clones displayed a 52-kDa protein band, which corresponded to a UGT1A1 control protein. Only four of the clones had a protein band that corresponded to the CYP1A2 control protein. Correct fragment size of the cDNAs in the remaining four clones was confirmed by RT-PCR and quantification of the mRNA product was accomplished by real-time RT-PCR. Expression of UGT1A1 in the transfected cells was 10(4)-10(5)-fold higher relative to the UV5P3 parental cells. One clone (#14) had a 10-fold higher increase in expression at 1.47 x 10(5) over the other three clones. This clone was also the most active in converting N-hydroxy-PhIP to N-hydroxy-PhIP glucuronide conjugates in microsomal metabolism assays. Based on the D50 values, the cytotoxic effect of PhIP was decreased approximately 350-fold in the 5P3hUGT1A1 cells compared to the UV5P3 control cells. In addition, no significant increase in mutation frequency was observed in the transfected cells. These results clearly indicate that UGT1A1 plays a critical role in PhIP biotransformation, providing protection against PhIP-mediated cytotoxicity and mutagenicity.

Animals↗