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1.
  • Laryea, Daniel, 1948- (författare)
  • Inhibitory action of benzimidazole fungicides on the in vivo incorporation of [3H]thymidine in various organs of the mouse
  • 1990
  • Ingår i: Food and Chemical Toxicology. - 0278-6915 .- 1873-6351. ; 10:28, s. 701-706
  • Tidskriftsartikel (refereegranskat)abstract
    • The effect of benomyl on the DNA turnover in various organs of the mouse was evaluated by measuring the incorporation of [3H]thymidine 24 hr after oral administration of different doses (1.3, 2.55 and 5.1 nmol/kg body weight) of benomyl. In the thymus, spleen and testis there was a clear relationship between dose and effect, the no-observed-effect level being 1.3 mmol/kg body weight. However, in the liver and kidney there was no obvious relationship between dose and effect, the [3H]thymidine incorporation being inhibited even at the lowest dose. Equimolar amounts of the closely related fungicide carbendazim inhibited the [3H]thymidine incorporation only in the testis. The observed differences between the two compounds was not a result of different absorption rates. Whole-body autoradiography indicated a rapid absorption and a similar distribution pattern for [phenyl(U)-14C)benomyl and [phenyl(U)-14C]carbendazim. Apart from an accumulation in the retina, liver and kidney, most other organs were almost devoid of [14C]benomyl- and [14C]carbendazim-associated radioactivity.
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2.
  • Skog, K, et al. (författare)
  • Polar and non-polar heterocyclic amines in cooked fish and meat products and their corresponding pan residues
  • 1997
  • Ingår i: Food and Chemical Toxicology. - 0278-6915 .- 1873-6351. ; 35:6, s. 555-565
  • Tidskriftsartikel (refereegranskat)abstract
    • Fourteen cooked dishes with their corresponding pan residues were analysed for polar and non-polar heterocyclic amines using HPLC. The choice of foods, including beef, pork, poultry, game, fish, egg and sausages, was based on an investigation of an elderly population in Stockholm participating in an analytical epidemiological case-control study on cancer risks after intake of heterocyclic amines. The food items were prepared using normal household cooking practices, and to reflect the wide range of surface browning of the cooked dishes that would be encountered in this population, four cooking temperatures were used in the range 150-225 degrees C. For all food samples, the total amount of heterocyclic amines formed at 150 degrees C was less than 1 ng/g cooked product, and at 175 degrees C less than 2 ng/g. The highest concentrations of heterocyclic amines were detected in fillet of pork, reindeer meat and chicken breast fried at 200 and 225 degrees C and their corresponding pan residues. The total sum of 2-amino-3,8-dimethylimidazo-[4,5-f]quinoxaline 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine was about 1 mu g per 100 g portion (including pan residues) for reindeer meat and chicken breast, and between 1.9 and 6.3 mu g per 100-g portion for fillet of pork. PhIP was the most abundant heterocyclic amine, identified in 73 of 84 samples, and the highest concentration of PhIP, 32.0 ng/g, was found in the pan residue from fillet of pork cooked at 225 degrees C. The non-polar heterocyclic amines 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole and 3-amino-1-methyl-5H-pyrido[4,3-b]indole were detected in the range of 0.5-7.4 ng/g in most foods cooked at 225 degrees C, and also in meat sauce prepared at 200 and 175 degrees C. The other heterocyclic amines tested for: 2-amino-3-methylimidazo- [4,5-f]quinoline, 2-amino-3,4-dimethylimidazo[4,5-f]quinoline, 2-amino-6-methyl-pyrido-[1,2-a:3',2'-d]-imidazole and 2-aminodipyrido-[1,2-a:3',2'-d]imidazole were present only at very low or non-detectable levels. The low recoveries of the amino-alpha-carbolines 2-amino-9H-pyrido[2,3-b]indole and 2-amino-3-methyl-9H-pyrido[2,3-b]indole made it impossible to quantify them. However, the co-mutagenic substances 1-methyl-9H-pyrido-[3,4-b]indole and 9H-pyrido[3,4-b]indole were detected at levels of about 1-30 ng/g in most of the dishes cooked at 200 and 225 degrees C. 
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3.
  • Thuvander, A., et al. (författare)
  • Levels of ochratoxin A in blood from Norwegian and Swedish blood donors and their possible correlation with food consumption
  • 2001
  • Ingår i: Food and Chemical Toxicology. - 0278-6915 .- 1873-6351. ; 39:12, s. 1145-1151
  • Tidskriftsartikel (refereegranskat)abstract
    • Blood levels of ochratoxin A were determined in 406 Scandinavian blood donors (206 from Oslo, Norway, and 200 from Visby on the island of Gotland, Sweden), using an HPLC method. In connection with the blood collection, the subjects were asked to fill in a food questionnaire to obtain individual dietary information relevant to ochratoxin A exposure. The mean plasma level of ochratoxin A was 0.18 ng/ml in Oslo and slightly higher, 0.21 ng/ml (P = 0.046) in Visby. There was no correlation between plasma levels of ochratoxin A and the estimated total dietary intake of ochratoxin A based on consumption data and levels in food (retrieved from the literature), neither was the plasma level of ochratoxin A correlated with the total amount of food consumed. However, consumption of several foods, including cereal products, wine, beer and pork, were to some minor degree related to high plasma levels of ochratoxin A. The strongest correlations (correlation coefficient r >0.4; P <0.001) were observed for women in relation to the consumption of beer or medium brown bread. Correlation analysis of combinations of two or more food categories did not result in any statistically significant correlation.
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4.
  • Aasa, Jenny, et al. (författare)
  • Cancer risk estimation of glycidol based on rodent carcinogenicity studies, a multiplicative risk model and in vivo dosimetry
  • 2019
  • Ingår i: Food and Chemical Toxicology. - : Elsevier BV. - 0278-6915 .- 1873-6351. ; 128, s. 54-60
  • Tidskriftsartikel (refereegranskat)abstract
    • Here we evaluate a multiplicative (relative) risk model for improved cancer risk estimation of genotoxic compounds. According to this model, cancer risk is proportional to the background tumor incidence and to the internal dose of the genotoxic compound. Furthermore, the relative risk coefficient per internal dose is considered to be approximately the same across tumor sites, sex, and species. In the present study, we demonstrate that the relative risk model is valid for cancer risk estimation of glycidol, a common food contaminant. Published tumor data from glycidol carcinogenicity studies in mice and rats were evaluated in combination with internal dose estimates from hemoglobin adduct measurements in blood from mice and rats treated with glycidol in short-term studies. A good agreement between predicted and observed tumor incidence in responding sites was demonstrated in the animals, supporting a relative risk coefficient that is independent of tumor site, sex, and species. There was no significant difference between the risk coefficients for mice (5.1% per mMh) and rats (5.4% per mMh) when considering internal doses of glycidol. Altogether, this mechanism-based risk model gives a reliable risk coefficient, which then was extrapolated to humans considering internal dose, and background cancer incidence.
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5.
  • Aasa, Jenny, et al. (författare)
  • Measurement of micronuclei and internal dose in mice demonstrates that 3-monochloropropane-1,2-diol (3-MCPD) has no genotoxic potency in vivo
  • 2017
  • Ingår i: Food and Chemical Toxicology. - : Elsevier BV. - 0278-6915 .- 1873-6351. ; 109, s. 414-420
  • Tidskriftsartikel (refereegranskat)abstract
    • In this study 3-monochloropropane-1,2-diol (3-MCPD), a compound that appears as contaminant in refined cooking oils, has been studied with regard to genotoxicity in vivo (mice) with simultaneous measurement of internal dose using state-of-the-art methodologies. Genotoxicity (chromosomal aberrations) was measured by flow cytometry with dual lasers as the frequency of micronuclei in erythrocytes in peripheral blood from BalbC mice intraperitoneally exposed to 3-MCPD (0, 50, 75, 100, 125 mg/kg). The internal doses of 3-MCPD in the mice were calculated from N-(2,3-dihydroxypropyl)-valine adducts to hemoglobin (Hb), quantified at very low levels by high-resolution mass spectrometry.Convincing evidence for absence of genotoxic potency in correlation to measured internal doses in the mice was demonstrated, despite relatively high administered doses of 3-MCPD. The results are discussed in relation to another food contaminant that is formed as ester in parallel to 3-MCPD esters in oil processing, i.e. glycidol, which has been studied previously by us in a similar experimental setup. Glycidol has been shown to be genotoxic, and in addition to have ca. 1000 times higher rate of adduct formation compared to that observed for 3-MCPD. The conclusion is that at simultaneous exposure to 3-MCPD and glycidol the concern about genotoxicity would be glycidol.
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6.
  • Aasa, Jenny, et al. (författare)
  • The genotoxic potency of glycidol established from micronucleus frequency and hemoglobin adduct levels in mice
  • 2017
  • Ingår i: Food and Chemical Toxicology. - : Elsevier BV. - 0278-6915 .- 1873-6351. ; 100, s. 168-174
  • Tidskriftsartikel (refereegranskat)abstract
    • Glycidol is a genotoxic animal carcinogen that has raised concern due to its presence in food, as glycidyl fatty acid esters. Here we investigated the genotoxicity of glycidol in BalbC mice (0-120 mg/kg) by monitoring the induction of micronuclei in peripheral blood as a marker of chromosomal damage. The scoring of the micronuclei was assessed by flow cytometry. In the treated mice, the internal dose of glycidol, expressed as area under the concentration-time curve, AUC (mol x L-1 x h; Mh), was measured by dihydroxypropyl adducts to hemoglobin (Hb). The study showed that glycidol induced linear dose dependent increases of Hb adducts (20 pmol/g Hb per mg/kg) and of micronuclei frequencies (12 parts per thousand per mMh). Compared to calculations based on administered dose, an improved dose-response relationship was observed when considering internal dose, achieved through the applied combination of sensitive techniques used for the scoring of micronuclei and AUC estimation of glycidol in the same mice. By comparing with earlier studies on micronuclei induction in mice exposed to ionizing radiation we estimated the radiation dose equivalent (rad-eq.) of glycidol to be ca 15 rad-eq./mMh.
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7.
  • Abramsson-Zetterberg, Lilianne (författare)
  • Strongly heated carbohydrate-rich food is an overlooked problem in cancer risk evaluation
  • 2018
  • Ingår i: Food and Chemical Toxicology. - : Elsevier BV. - 0278-6915 .- 1873-6351. ; 121, s. 151-155
  • Tidskriftsartikel (refereegranskat)abstract
    • A cascade of compounds is produced when foodstuffs are heated at high temperatures but only a few of these compounds have been identified and quantified. In this study data are evaluated regarding differences in the micronucleus frequency of human erythrocytes (fMNs) in peripheral blood (a known biomarker of genotoxicity) in individuals that consumed either high- or low-heated food during a 4-day period. Concomitantly, acrylamide (aa) levels were measured in the food that the participants consumed. The obtained fMNs in this human study are compared with the fMNs in mice after comparable exposure levels of pure aa. The results of this comparison showed several hundred times higher fMNs in humans compared with mice. With an assumed linear correlation between an increased genotoxic effect and cancer, our data suggest that aa only represents a fraction of all carcinogenic compounds produced in heated carbohydrate-rich food. Consequently, our daily intake of carbohydrate-rich food heated at high temperatures might be responsible for one-fifth of the rate of the total cancer risk. One sentence summary: A biomarker of genotoxicity indicates the risk of cancer to be some hundred-fold greater in heated carbohydrate-rich food than the risk calculated from animal studies on pure acrylamide.
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8.
  • Abramsson-Zetterberg, Lilianne, et al. (författare)
  • The synthetic food colouring agent Allura Red AC (E129) is not genotoxic in a flow cytometry-based micronucleus assay in vivo
  • 2013
  • Ingår i: Food and Chemical Toxicology. - : Elsevier BV. - 0278-6915 .- 1873-6351. ; 59, s. 86-89
  • Tidskriftsartikel (refereegranskat)abstract
    • The safety of several azo colouring agents, used as food additives, has during the years been questioned. Allura Red AC (E129) has in some publications been classified as genotoxic. In fact, in the European Union, Allura Red is permitted as a food additive in human food, but, surprisingly, it was not acceptable as an additive for use in animal feed. In this study we have evaluated whether Allura Red is genotoxic using a flow cytometer-based micronucleus assay in peripheral blood of mice. Male FVB mice were given a single intra-peritoneal injection of various doses of Allura Red and sacrificed at 46 h after treatment. The tested doses were 0, 100, 200, 400, 600, 800, 1000, 1500, and 2000 mg/kg body weight (b.w.). Each dose group constituted three mice, except for in the dose group of 1000 mg/kg b.w., which constituted four mice. Blood samples were collected and the frequency of micronucleated polychromatic erythrocytes (fMNPCE) and the cell proliferation (%PCE) was determined. The analyses did not show any significant difference in the %PCE or in the fMNPCE. Consequently, under the testing circumstances one can conclude that Allura Red is not genotoxic.
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9.
  • Alderborn, Anders, et al. (författare)
  • Genetically modified plants for non-food or non-feed purposes : straightforward screening for their appearance in food and feed
  • 2010
  • Ingår i: Food and Chemical Toxicology. - : Elsevier BV. - 0278-6915 .- 1873-6351. ; 48:2, s. 453-464
  • Tidskriftsartikel (refereegranskat)abstract
    • Genetically modified (GM) plants aimed at producing food/feed are part of regular agriculture in many areas of the World. Commodity plants have also found application as bioreactors, designated non-food/non-feed GM (NFGM) plants, thereby making raw material for further refinement to industrial, diagnostic or pharmaceutical preparations. Many among them may pose health challenge to consumers or livestock animals, if occurring in food/feed. NFGM plants are typically released into the environment, but are grown under special oversight and any among several containment practices, none of which provide full protection against accidental dispersal. Adventitious admixture with food or feed can occur either through distributional mismanagement or as a consequence of gene flow to plant relatives. To facilitate NFGM surveillance we propose a new mandatory tagging of essentially all such plants, prior to cultivation or marketing in the European Union. The suggested tag--Plant-Made Industrial or Pharmaceutical Products Tag (PMIP-T)--is envisaged to occur as a transgenic silent DNA identifier in host plants and designed to enable technically simple identification and characterisation of any NFGM. Implementation of PMIP-T would permit inexpensive, reliable and high-throughput screening for NFGM specifically. The paper outlines key NFGM prospects and challenges as well as the PMIP-T concept.
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10.
  • Andersson, Maria A., et al. (författare)
  • Evaluation of the potential genotoxicity of chromium picolinate in mammalian cells in vivo and in vitro
  • 2007
  • Ingår i: Food and Chemical Toxicology. - : Elsevier BV. - 0278-6915 .- 1873-6351. ; 45:7, s. 1097-1106
  • Tidskriftsartikel (refereegranskat)abstract
    • Chromium picolinate (CrPic) is a synthetic nutritional supplement primarily used for weight loss and muscle building. Recent studies have indicated that CrPic might be genotoxic and these findings together with the wide-spread consumer use, have increased the concern about its safety. In the present study we investigated the potential genotoxicity of CrPic in mice given a single intraperitoneal injection (up to 3 mg/kg b.wt.) by evaluating the frequency of micronucleated polychromatic erythrocytes (fMNPCE) in peripheral blood, and DNA damage in lymphocytes and hepatocytes. The fMNPCE was evaluated after 42 h and DNA damage after 16 h. Using the Comet assay DNA damage was also monitored in extended-term cultures of human lymphocytes and in L5178Y mouse lymphoma cells that had been exposed for 3 h to 500 μM CrPic under different exposure conditions.A slight, but significant CrPic-induced increase in DNA damage (P < 0.001) was observed in the human lymphocytes, but only when these cells were exposed in the absence of serum. In all other experiments CrPic was found to be without genotoxic effects, both in vivo and in vitro. Taken together, our results suggest that a high concentration of CrPic might be DNA damaging, but only under non-physiological conditions.
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