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At least 19 recordsLinked to original sources
PubMed2005

Controlling acrylamide in French fry and potato chip models and a mathematical model of acrylamide formation: acrylamide: acidulants, phytate and calcium.

We previously reported that in potato chip and French fry models, the formation of acrylamide can be reduced by controlling pH during processing steps, either by organic (acidulants) or inorganic acids. Use of phytate, a naturally occurring chelator, with or without Ca++ (or divalent ions), can reduce acrylamide formation in both models. However, since phytate itself is acidic, the question remains as to whether the effect of phytate is due to pH alone or to additional effects. In the French fry model, the effects on acrylamide formation of pH, phytate, and/or Ca++ in various combinations were tested in either blanching or soaking (after blanching) steps. All treatments significantly reduced acrylamide levels compared to control. Among variables tested, pH may be the single most important factor for reducing acrylamide levels, while there were independent effects of phytate and/or Ca++ in this French fry model. We also developed a mathematical formula to estimate the final concentration of acrylamide in a potato chip model, using variables that can affect acrylamide formation: glucose and asparagine concentrations, cut potato surface area and shape, cooking temperature and time, and other processing conditions.

Acids↗
PubMed1986

Effect of single and repeated doses of acrylamide and bis-acrylamide on glutathione-S-transferase and dopamine receptors in rat brain.

The effect of single and repeated doses of acrylamide (a neurotoxin) and N,N'-methylene-bis-acrylamide (a non-neurotoxic analogue of acrylamide) on glutathione (GSH), glutathione-S-transferase (GST) and dopamine receptors has been studied in rat brain. In vitro, both acrylamide and bis-acrylamide decreased brain GSH content in a concentration-dependent manner. At equimillimolar concentrations (2-10 mM) bis-acrylamide was more effective than acrylamide in lowering GSH levels. In vitro, GST activity was also inhibited as a function of acrylamide concentration. A single dose of either acrylamide or bis-acrylamide depleted GSH content of rat brain in a concentration-dependent manner without inhibiting GST activity. Repeated administration of either acrylamide or bis-acrylamide in rats (50 mg/kg X 10 days) decreased GSH content in the brain but GST activity was inhibited only by acrylamide and not by bis-acrylamide. Single or repeated injections of acrylamide but not of bis-acrylamide increased brain dopamine receptors ([3H]spiroperidol binding) in a concentration-dependent manner.

Acrylamide↗
PubMed2004

Estimation of the dietary intake of acrylamide by German infants, children and adolescents as calculated from dietary records and available data on acrylamide levels in food groups.

Dietary intakes of acrylamide for the general population were estimated by FAO/WHO to be in the range of 0.3 to 0.8 microg/(kg(bw) *d). It was supposed that children and adolescents would generally have intakes twice to three times higher than adults. However, relevant data is rare. Therefore, 3- or 7-day dietary records (n = 2956) from infants, children and adolescents aged 0.5 to 18 years from the DONALD study (2001) and other studies (RUB studies) were evaluated to estimate the potential dietary intake of acrylamide. Statistical data of the intake of 6 food groups relevant for acrylamide exposure were combined with available data for ranges of acrylamide concentrations in more than 1500 foods in Germany. Scenarios were calculated assuming minimum, median and maximum acrylamide concentration in food groups. Assuming median (minimum; maximum) acrylamide concentrations in foods and mean consumed food amounts, the calculated intake of acrylamide ranged from 0.21-0.43 (0.12-0.19; 0.98-1.79) microg/(kg(bw) *d) between the age groups from <1 to <19 years in the DONALD study and was 0.61 (0.21; 2.58) microg/(kg(bw) *d) from 1 to <7 years in the RUB studies. The highest intake was calculated for children aged 1-<7 years. The highest proportions of total intake of acrylamide came from the intake of commercial baby food (86-91%) in infants, and bread (18-46%), pastries (16-35%), and potato products (7-35%) in children and adolescents, depending on scenario and age. Our estimated data are in the range of reports from the literature for adolescents and adults in Germany and other European countries and lower than reports for infants. Our results do not confirm that children and adolescents will have higher exposures to acrylamide than adults. Practical suggestions to lower the risk of acrylamide exposure by food without decreasing the quality of the nutrition in the diet are given.

Acrylamide↗
PubMed2005

Study of acrylamide in coffee using an improved liquid chromatography mass spectrometry method: Investigation of colour changes and acrylamide formation in coffee during roasting.

An improved analytical method for the determination of acrylamide in coffee is described using liquid chromatography coupled to mass spectrometric detection (LC-MS). A variety of instant, ground and laboratory roasted coffee samples were analysed using this method. The sample preparation entails extraction of acrylamide with methanol, purification with Carrez I and II solutions, evaporation and solvent change to water, and clean-up with an Oasis HLB solid-phase extraction (SPE) cartridge. The chromatographic conditions allowed separation of acrylamide and the remaining matrix co-extractives with accurate and precise quantification of acrylamide during MS detection in SIM mode. Recoveries for the spiking levels of 50, 100, 250 and 500?microg/kg ranged between 99 and 100% with relative standard deviations of less than 2%. The effects of roasting on the formation of acrylamide and colour development were also investigated at 150, 200 and 225 degrees C. Change in the CIE (Commission Internationale de l'Eclairage) a* colour value was found to show a good correlation with the change in acrylamide. CIE a* and acrylamide data was fitted to a non-linear logarithmic function for the estimation of acrylamide level in coffee. Measured acrylamide levels in commercial roasted coffees compared well with the predicted acrylamide levels from the CIE a* values.

Acrylamide↗
PubMed2005

The acrylamide intake via some common baby food for children in Sweden during their first year of life--an improved method for analysis of acrylamide.

The acrylamide levels in breast milk and the main categories of Swedish baby food products, i.e. breast milk substitute (infant formula), gruel, porridge and canned baby food, have been analysed. Furthermore, the acrylamide intake from these products by children up to one year of age has been estimated. Other kind of foods e.g. biscuits, are not included. Because of the expected low concentrations of acrylamide, a new sample extraction method for detection by liquid chromatography, tandem mass spectrometry, was developed and validated. The lower limit of quantification was 0.5 microg kg(-1) for liquid samples and 2 microg kg(-1) for other samples. The average levels found for gruel, porridge and canned baby food, all ready to eat, were 1.4, 26, and 7.8 microg/kg respectively. We found great variations in the acrylamide levels between and in different food categories, <0.5-64 microg/kg. For all breast milk samples except one the acrylamide level was below the limit of quantification (0.5 microg/kg). In three out of eight analysed samples of breast milk substitute, the acrylamide content was verified and possible to quantify. Assuming an acrylamide level of 0.25 microg/kg in breast milk, the mean acrylamide intake during the first six months for children who were exclusively breast-fed was estimated to be 0.04 microg/kg b.w./day. The mean acrylamide intake from breast milk and commercially made baby food during the whole first year varies due to the length of breast-feeding and the choice of baby food. The intake level range was estimated to be 0.04-1.2 microg/kg b.w/day. The mean intake between seven and twelve months of age was estimated to be about 0.5 microg/kg b.w./day.

Acrylamide↗
PubMed2006

Toxicokinetics of acrylamide in humans after ingestion of a defined dose in a test meal to improve risk assessment for acrylamide carcinogenicity.

High amounts of acrylamide in some foods result in an estimated daily mean intake of 50 microg for a western style diet. Animal studies have shown the carcinogenicity of acrylamide upon oral exposure. However, only sparse human toxicokinetic data is available for acrylamide, which is needed for the extrapolation of human cancer risk from animal data. We evaluated the toxicokinetics of acrylamide in six young healthy volunteers after the consumption of a meal containing 0.94 mg of acrylamide. Urine was collected up to 72 hours thereafter. Unchanged acrylamide, its mercapturic acid metabolite N-acetyl-S-(2-carbamoylethyl)cysteine (AAMA), its epoxy derivative glycidamide, and the respective metabolite of glycidamide, N-acetyl-S-(2-hydroxy-2-carbamoylethyl)cysteine (GAMA), were quantified in the urine by liquid chromatography-mass spectrometry. Toxicokinetic variables were obtained by noncompartmental methods. Overall, 60.3 +/- 11.2% of the dose was recovered in the urine. Although no glycidamide was found, unchanged acrylamide, AAMA, and GAMA accounted for urinary excretion of (mean +/- SD) 4.4 +/- 1.5%, 50.0 +/- 9.4%, and 5.9 +/- 1.2% of the dose, respectively. Apparent terminal elimination half-lives for the substances were 2.4 +/- 0.4, 17.4 +/- 3.9, and 25.1 +/- 6.4 hours. The ratio of GAMA/AAMA amounts excreted was 0.12 +/- 0.02. In conclusion, most of the acrylamide ingested with food is absorbed in humans. Conjugation with glutathione exceeds the formation of the reactive metabolite glycidamide. The data suggests an at least 2-fold and 4-fold lower relative internal exposure for glycidamide from dietary acrylamide in humans compared with rats or mice, respectively. This should be considered for quantitative cancer risk assessment.

Absorption↗
PubMed2005

Acrylamide in Japanese processed foods and factors affecting acrylamide level in potato chips and tea.

Acrylamide concentrations in processed foods sold in Japanese markets were analyzed by LC-MS/MS and GC-MS methods. Most potato chips and whole potato-based fried snacks showed acrylamide concentration higher than 1000 microg/kg. The concentrations in non-whole potato based Japanese snacks, including rice crackers and candied sweet potatoes, were less tha. 350 microg/kg. Those in instant precooked noodles were less than 100 microg/kg with only one exception. The effect of storage condition of potato tubers on acrylamide concentration in potato chips after frying was also investigated. Sugar content in the tubers increased during cold storage, and the acrylamide concentration increased accordingly. The concentrations of asparagine and other amino acids, however, did not change during the cold storage. High correlations were observed between the acrylamide content in the chips and glucose and fructose contents in the tubers. This fact indicated that the limiting factor for acrylamide formation in potato chips is reducing sugar, not asparagine content in the tubers. Effects of roasting time and temperature on acrylamide concentration in roasted green tea are also described.

Acrylamide↗
PubMed1981

Neurotransmitter receptors in brain regions of acrylamide- treated rats. II: Effects of extended exposure to acrylamide.

Acrylamide was administered orally to 6 week old male rats in ten doses, spread over a two week period. At the two lower doses (5 and 10 mg/kg, total dose 50 and 100 mg/kg) effects on neurotransmitter receptor sites appeared confined to the striatum where both the dopamine and muscarinic acetylcholine receptors exhibited enhanced binding twenty four hours after the last acrylamide dose. Other receptor sites within the frontal cortex, cerebellum, and medulla were not significantly altered. At the highest dose (20 mg/kg, given ten times), increases were also found for frontal cortical serotonin, medullary glycine, and cerebellar GABA receptor sites. The only unaffected receptor found was the cortical site for benzodiazepene. One week after the final acrylamide dose, the intensity of binding of all ligands studied was not significantly different in treated and control groups. Thus, effects appeared reversible. Since striatal membrane protein concentration was reduced by treatment of rats with acrylamide, the observed increased in activity of muscarinic receptors could be best accounted for in terms of loss of striatal non-receptor protein rather than increased binding. However, the magnitude of increased striatal 3H-spiroperidol binding in treated animals suggested an increase in overall binding capacity. An effect on dopamine neurons was also suggested by a decreased responsiveness to apomorphine in rats treated with acrylamide at 10 mg/kg for 10 successive days; however, the effect had dissipated by 8 days after the final injection of acrylamide.

Acrylamides↗
PubMed1979

[Lipoprotein electrophoresis on acrylamide-agarose plates, with discontinuous acrylamide gradient].

We describe a modified lipoprotein electrophoresis on acrylamide gel. The lipoproteins, prestained with Sudan Black, are separated by running on acrylamide-agarose gels, with two different concentrations of acrylamide and a constant concentration of agarose. The sera are deposited in the first gel (2% acrylamide). Chylomicrons remain at origin and other lipoproteins run through the first gel to the second one (3% acrylamide gel). VLDL stays at the junction of both gels, LDL and HDL are separated in the 3% acrylamide gel. By this technique, we were able to detect an increase of Lp(a) and to identify the different types of hyperlipoproteinemia. After running, the plates can be treated for storage.

Electrophoresis, Agar Gel↗
PubMed1990

Effects of acrylamide and N,N'-methylene-bis-acrylamide on creatine kinase activity.

In vitro, both acrylamide and N,N'-methylene-bis-acrylamide inhibited creatine kinase (CK) activity from brain or sciatic nerve with almost the same potency. In vivo, only acrylamide (50 mg/kg b. wt./day, 8 days) caused paralysis of hind limbs and suppressed CK activity in cerebrum, cerebellum, spinal cord and muscle in rats. Bis-acrylamide (50 mg or 100 mg/kg b. wt./day, 8 days) caused no paralysis nor inhibition of CK activity in any tissue examined. Definite inhibition of CK was not found in sciatic nerve from rats given either chemical. The inhibition of CK may play a role in the genesis of toxicity of acrylamide especially in the central nervous system.

Acrylamide↗
PubMed1981

Neurotransmitter receptors in brain regions of acrylamide- treated rats. I: Effects of a single exposure to acrylamide.

A single oral dose of acrylamide (25 or 50 mg/kg) increased the level of striatal 3H-spiroperidol binding in six week old male rats. This enhanced dopamine receptor activity was specific since treatment caused no significant changes in glycine, serotonin, and muscarinic cholinergic binding. At the highest acrylamide dose tested (100 mg/kg), elevations of the medullary glycine and frontal cortical serotonin receptors were also found. Pretreatment of animals with a blocker of hepatic mixed function oxidase (SKF 525a) or a thiol blocker (methylmercuric chloride) prevented the acrylamide-induced elevation of striatal spiroperidol binding, indicating that the causative agent was a secondary metabolite of acrylamide. Apomorphine-induced motility was significantly attenuated by 24 hr predosing with acrylamide, suggesting a change in the sensitivity of the dopamine receptor. The behavioral relevance of observed biochemical changes was thus shown by the altered response of treated animals to apomorphine.

Acrylamides↗
PubMed2005

Mercapturic acids of acrylamide and glycidamide as biomarkers of the internal exposure to acrylamide in the general population.

Acrylamide (AA), a widely used industrial monomer which is categorised to be carcinogenic, was found to be generated in starch-containing foods during the heating process. This discovery has caused reasonable concern about possible health risks to humans due to dietary acrylamide uptake. In order to gain more information on human metabolism of acrylamide and to contribute to the assessment of the human carcinogenic risk due to AA uptake we measured the mercapturic acid of AA and its epoxide glycidamide (GA) i.e. N-acetyl-S-(2-carbamoylethyl)-L-cysteine (AAMA) and N-(R,S)-acetyl-S-(2-carbamoyl-2-hydroxyethyl)-L-cysteine (GAMA) in human urine. The relation between AAMA and GAMA is important in this context because GA is thought to be the ultimate carcinogenic metabolite of AA. The median levels in smokers (n=13) were found to be about four times higher than in non-smokers (n=16) with median levels of 127 microg/l versus 29 microg/l for AAMA and 19 microg/l versus 5 microg/l for GAMA. Therefore cigarette smoke proved to be an important source of acrylamide exposure. The level of AAMA in the occupationally non-exposed collective (n=29) ranged from 3 to 338 microg/l, the level of GAMA from <LOD to 45 microg/l. The ratio of GAMA:AAMA varied from 0.03 to 0.53, median was 0.16 which is in reasonable agreement with results of different studies on rats. Thus the metabolic conversion of acrylamide to its genotoxic epoxide glycidamide seems to occur to a comparable extent in rats and humans. Consequently, risk estimations by various authorities based on experimental data obtained in rats are supported by our findings. Besides we also measured the haemoglobin adducts of AA and GA in the blood of 26 participants. From these results compared to the mercapturic acids, we deduce a steady state for AA uptake, and we demonstrate a higher reactivity of GA in comparison to AA towards haemoglobin compared to glutathione in humans.

Acetylcysteine↗
PubMed1975

Neurotoxicity of acrylamide and its analogues and effects of these analogues and other agents on acrylamide neuropathy.

N-Hydroxymethylacrylamide, N-methylacrylamide, and N,N-diethylacrylamide produce peripheral neuropathy in rats. Seven other compounds related to acrylamide do not produce neuropathy. Rats given one of the three neurotoxic compounds are more susceptible to acrylamide. A regime for testing acrylamide analogues for neuro-toxicity is suggested. DDT, phenobarbitone, or high dietary concentrations of vitamin A or E have no effect on the development of acrylamide neuropathy in rats. Acrylamide produces neuropathy in hens but not in frogs or goldfish.

Acrylamides↗
PubMedDate not supplied

Molecular modeling of acrylamide derivatives: the case of N-acryloylaminoethoxyethanol versus acrylamide and trisacryl.

Molecular mechanics (for evaluation of total energies of individual structures of monomers and oligomers) and molecular dynamics (for evaluating dynamic dependencies of structural features) were used for obtaining information on some unique chemical behavior of a novel N-substituted acrylamide (N-acryloylaminoethoxyethanol; AAEE) vs. conventional acrylamide and trisacryl (N-acryloyl-2-amino-2-hydroxymethyl-1,3-propane diol, an extremely hydrophilic derivative; Tris-A). As free monomers, Tris-A degrades with zero-order and acrylamide with first-order kinetics, whereas AAEE is highly resistant to hydrolysis. It is found that Tris-A (and its dideoxy derivative) is constantly forming hydrogen bonds between the -OH groups and the carbonyl of the amido group (bond distances of 1.64 to 1.70 A); this activates a mechanism of "N-O acyl transfer" which leads to quick degradation of the amido bond even under mildly alkaline conditions. Conversely, AAEE (which also contains an omega-OH group increasing its hydrophilicity) has no tendency to form H-bonds with the amido carbonyl, thus being resistant to the above degradation mechanism. In fact, the oxygen in the ethoxy moiety of the N-substituent chain acts as a preferential partner for H-bond formation with the omega-OH group. In the oligomeric state, it is found that Tris-A (tetrameric and dodecameric structures were simulated) tends to form inter-residue H-bonds (approximately parallel to the growing chain) competing with the intra-residue H-bonds (folding onto the amido carbonyl and approximately perpendicular to the oligomer chain), thus greatly increasing its stability.(ABSTRACT TRUNCATED AT 250 WORDS)

Acrylamide↗
PubMed2005

Kinetic and mechanistic data needs for a human phsiologically based pharmacokinetic (PBPK) model for acrylamide: pharmacokinetic model for acrylamide.

A pharmacokinetic (PBPK) model has been developed for acrylamide (AMD) and its oxidative metabolite, glycidamide (GLY), in the rat based on available information. Despite gaps and limitations to the database, model parameters have been estimated to provide a relatively consistent description of the kinetics of acrylamide and glycidamide using a single set of values (with minor adjustments in some cases). Future kinetic and mechanistic studies will need to focus on the collection of key data for refining certain model parameters and for model validation, as well as for conducting studies that elucidate the mechanism of action. Development of a validated human AMD/GLY PBPK model capable of predicting target tissue doses at relevant dietary AMD exposures, in combination with expanding data on modes of action, should allow for a substantive improvement in the risk assessment of acrylamide in food.

Acrylamide↗
PubMed2006

Preparation and application of poly(N,N-dimethylacrylamide-co-acrylamide) and poly(N-isopropylacrylamide-co-acrylamide)/kappa-Carrageenan hydrogels for immobilization of lipase.

In the present of this study, two novel polymeric matrixes that are poly(N,N-dimethylacrylamide-co-acrylamide) and poly(N-isopropylacrylamide-co-acrylamide)/kappa-Carrageenan was synthesized and applied for immobilization of lipase. For the immobilization of enzyme, two different immobilization procedures have been carried out via covalently binding and entrapment methods. On the free and immobilized enzymes activities, optimum pH, temperature, storage and thermal stability was investigated. The optimum temperature for free, covalently immobilized and entrapped enzymes was found to be 30, 35 and 30 degrees C, respectively. Optimum pH for both free and immobilized enzymes was also observed at pH 8. Maximum reaction rate (Vmax) and Michaelis-Menten constant (Km) were determined for free and immobilized lipases. Furthermore, the reuse numbers of immobilized enzymes also studied. It was observed that after 40th use in 5 days, the retained activities for covalently immobilized and entrapped lipases were found as 39% and 22%, respectively. Storage and thermal stability of enzyme was also increased by as a result of immobilization procedures.

Acrylamides↗
PubMed1989

Acrylamide derivatives as antiallergic agents. I. Synthesis and structure-activity relationships of N-[(4-substituted 1-piperazinyl)alkyl]-3-(aryl and heteroaryl)acrylamides.

A new series of acrylamide derivatives (7-10) were synthesized. Antiallergic activity of these compounds was evaluated and their structure-activity relationships were examined. Compound 10d, N-[4-(4-diphenylmethyl-1-piperazinyl)butyl]-3-(3-pyridyl)acrylamid e, showed antiallergic activity equivalent or superior to that of ketotifen in the rat passive cutaneous anaphylaxis (PCA) test by oral administration. Compound 10d, unlike ketotifen, had more potent in vitro 5-lipoxygenase inhibitory activity than caffeic acid, whereas its in vitro antihistamine activity was weaker than that of ketotifen. In addition, its inhibitory activity against histamine release from rat mast cells was approximately two-thirds as potent as that of disodium cromoglycate (DSCG). Compound 10d is a promising agent for treating a variety of allergic diseases.

Acrylamides↗
PubMed2002

Determination of acrylamide in foods by GC/MS using 13C-labeled acrylamide as an internal standard.

A method was developed for the determination of trace amounts of acrylamide (AA) in foods. The method includes the addition of 13C-labeled acrylamide-1-13C (AA-1-13C) as an internal standard, extraction with water, bromination, clean-up with a Florisil cartridge column, dehydrobromination and GC/MS analysis in the selected ion monitoring (SIM) mode. Bromination of AA to 2,3-dibromopropionamide (2,3-DBPA) was done using potassium bromide and potassium bromate under an acidic condition. 2,3-DBPA was converted to 2-bromopropenamide (2-BPA) by dehydrobromination with triethylamine before GC/MS analysis. The recoveries of AA from spiked potato chips, corn snack, pretzel and roasted tea were 97-105%, and their relative standard deviations were 0.8-3.9%. The detection limit of AA in foods was 9 ng/g. The method was applied to thirty-one foods purchased from retail markets. AA was found in potato chips at the level of 466-3,340 ng/g, and in other foods at the level of ND-520 ng/g.

Acrylamide↗