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PubMed2003

Analysis of acrylamide by LC-MS/MS and GC-MS in processed Japanese foods.

Acrylamide concentrations in processed foods (63 samples covering 31 product types) from Japan were analysed by LC-MS/MS and GC-MS methods. The limit of detection and limit of quantification of acrylamide were 0.2 ng x ml(-1) (6 fmol) and 0.8 ng x ml(-1) (22 fmol), respectively, by LC-MS/MS, and those of 2,3-dibromopropionamide derived from acrylamide were 12 ng x ml(-1) (52 fmol) and 40 ng x ml(-1) (170 fmol), respectively, by GC-MS. Repeatability given as RSD was <5 and <15% for the LC-MS/MS and GC-MS methods, respectively. High correlation (r(2) - 0.946) was observed between values obtained by the two methods. Most potato crisps and whole potato-based fried snacks showed acrylamide concentrations >1000 microg x kg(-1). The concentrations in non-whole potato-based snacks, rice crackers processed by grilling or frying, and candied sweet potatoes were lower compared with those in the potato crisps and the whole potato-based fried snacks. One of the whole potato-based fried snacks, however, showed low acrylamide concentration (<50 microg x kg(-1)) suggesting the formation of acrylamide is strongly influenced by processing conditions. Acrylamide concentrations in instant precooked noodles and won-tons were <100 microg x kg(-1) with only one exception. Roasted barley grains for 'Mugi-cha' tea contained 200-600 microg x kg(-1) acrylamide.

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PubMed2006

Linear and non-linear kinetics in the synthesis and degradation of acrylamide in foods and model systems.

Isothermal acrylamide formation in foods and asparagine-glucose model systems has ubiquitous features. On a time scale of about 60 min, at temperatures in the approximate range of 120-160 degrees C, the acrylamide concentration-time curve has a characteristic sigmoid shape whose asymptotic level and steepness increases with temperature while the time that corresponds to the inflection point decreases. In the approximate range of 160-200 degrees C, the curve has a clear peak, whose onset, height, width and degree of asymmetry depend on the system's composition and temperature. The synthesis-degradation of acrylamide in model systems has been recently described by traditional kinetic models. They account for the intermediate stages of the process and the fate of reactants involved at different levels of scrutiny. The resulting models have 2-6 rate constants, accounting for both the generation and elimination of the acrylamide. Their temperature dependence has been assumed to obey the Arrhenius equation, i.e., each step in the reaction was considered as having a fixed energy of activation. A proposed alternative is constructing the concentration curve by superimposing a Fermian decay term on a logistic growth function. The resulting model, which is not unique, has five parameters: a hypothetical uninterrupted generation-level, two steepness parameters; of the concentration climbs and fall and two time characteristics; of the acrylamide synthesis and elimination. According to this model, peak concentration is observed only when the two time constants are comparable. The peak's shape and height are determined by the gap between the two time constants and the relative magnitudes of the two "rate" parameters. The concept can be extended to create models of non-isothermal acrylamide formation. The basic assumption, which is yet to be verified experimentally, is that the momentary rate of the acrylamide synthesis or degradation is the isothermal rate at the momentary temperature, at a time that corresponds to its momentary concentration. The theoretical capabilities of a model of this kind are demonstrated with computer simulations. If the described model is correct, then by controlling temperature history, it is possible to reduce the acrylamide while still accomplishing much of the desirable effects of a heat process.

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PubMed2003

Weak yet distinct mutagenicity of acrylamide in mammalian cells.

BACKGROUND: Despite concern raised with the announcement that common heating processes such as frying introduce acrylamide, a known rodent carcinogen, into food, the mutagenicity of acrylamide in mammalian DNA is controversial. METHODS: Big Blue mouse embryonic fibroblasts, which carry a lambda phage cII transgene, were treated with acrylamide. Formation of DNA adducts was determined by terminal transferase-dependent polymerase chain reaction. Mutational events were detected with a lambda phage-based mutagenesis assay and expressed as the frequency of the number of mutant cII plaques per total number of plaques screened. Mutations were confirmed by DNA sequence analysis. All statistical tests were two-sided. RESULTS: In vitro treatment of the cells with acrylamide at millimolar concentrations induced DNA adducts along the cII gene. Treatment with acrylamide at micromolar concentrations increased the frequency of mutations in the cII gene up to twofold relative to control treatment (13.8 x 10(-5), 95% confidence interval [CI] = 12.3 to 15.3 x 10(-5) versus 6.9 x 10(-5), 95% CI = 6.5 to 7.3 x 10(-5), df = 2, 21; P<.001; ANOVA). The specificity of acrylamide in inducing cII gene mutations was shown by a statistically significantly different mutational spectrum from that in control-treated cells, with an excess of G --> C transversions and A --> G transitions (P =.024; Adams and Skopek test). Although some of the frequently mutated sites in the cII gene co-localized with sites of preferential DNA adduct formation, there was no direct relationship. CONCLUSION: Acrylamide had distinct mutagenicity in transgenic mouse embryonic fibroblast cells, which might potentially be ascribed to its DNA adduct-inducing property. Whether acrylamide has the same effects on human cells is yet to be determined.

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PubMed1989

Acrylamide quenching of tryptophan photochemistry and photophysics.

Studies of acrylamide quenching of tryptophan (Trp) fluorescence, photochemistry, and photoionization have been conducted. Quenching of Trp fluorescence in aqueous solution by addition of acrylamide in the concentration range 0.0-0.5 M was measured and resulted in a Stern-Volmer quenching constant of KSV = 21 +/- 3 M-1. Photolysis experiments were performed in which Trp was photolyzed at 295 nm in the presence of varying concentrations of acrylamide. The loss of Trp was monitored using reverse-phase high performance liquid chromatography (RP-HPLC) and was observed to follow first order kinetics. Production of N-formylkynurenine (NFK) was observed by RP-HPLC in irradiated Trp samples both in the presence and absence of added acrylamide. In addition, no new photochemical product was detected. This was taken as evidence that acrylamide did not alter the photochemical pathway but just reduced the reaction rate as expected for a physical quenching mechanism. Plotting the reciprocal of photolysis rate constant versus acrylamide concentration produced a Stern-Volmer constant for quenching of Trp photochemistry of KSV = 6 +/- 2 M-1. The KSV values for both fluorescence quenching and photolysis quenching were thus large, implying efficient quenching of both processes by acrylamide. Assuming an excited singlet state lifetime of 2.8 ns, the calculated second-order quenching rate constants for fluorescence and photolysis were kq = 7.5 x 10(9) and 2.1 x 10(9) M-1 s-1 respectively. The possible involvement of photoionization in the photolysis mechanism was investigated by studies of acrylamide quenching of voltage transients produced by xenon flash lamp excitation of Trp at aqueous/teflon or aqueous/mica interfaces.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1978

The effect of acrylamide on human polymorphonuclear neutrophils in vitro.

Acrylamide (CH2CHCONH2), the vinyl monomer of the industrially useful polymer polyacrylamide, is a recognised neurotoxin. Investigation in our laboratory indicated that, in addition to its neurotoxic effect, acrylamide depressed human polymorphonuclear leucocyte (PMN) chemotaxis in vitro. As genetic or chemical inhibition of PMN phagocytic function frequently pre-disposes patients to repeated bacterila infections, the in vitro effects of acrylamide on several other human PMN functions were studied. Acrylamide in concentrations up to 37.5 mg/ml had no effect on trypan blue uptake. However, bacterial ingestion, killing, and induced chemiluminescence were depressed by pre-treatment with acrylamide (10 mg/ml). It seems unlikely that acrylamide exposure alters host resistance to bacterial infections, because (a) large doses of acrylamide are necessary to interfere with phagocytic functions, (b) acrylamide reacts readily with proteins on many tissue cells and may be made inaccessible or non-toxic to PMN'S and (C) PMNs have a rapid turnover rate in the body and non-functional cells would be rapidly replaced by functional cells.

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PubMed2002

Acrylamide: increased concentrations in homemade food and first evidence of its variable absorption from food, variable metabolism and placental and breast milk transfer in humans.

We have developed a liquid chromatography/mass spectrometry (LC-MS/MS) assay to determine acrylamide in various body fluids. The assay also allows the reliable quantitation of acrylamide in food. In a total of 11 healthy male and female subjects, we were able to show that acrylamide from food given to humans is in fact absorbed from the gut. The half-lives determined in two male subjects were 2.2 and 7 h. Acrylamide was found in human breast milk and penetrated the human placenta (n = 3). The variability of acrylamide concentrations found in this investigation is most likely caused by variable intersubject bioavailability and metabolism. This may be an important indication that the assessment of the risk from acrylamide for the individual may be very difficult without knowing the concentrations of acrylamide in the body. This should be considered in the design of any risk assessment study or post hoc analysis of earlier studies. At this time, we suggest that pregnant women and breast-feeding mothers avoid acrylamide-containing food.

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PubMed2005

Influence of diet on exposure to acrylamide--reflections on the validity of a questionnaire.

AIM: This pilot study attempts to assess how far the standardized questionnaires are a valid tool to detect the food-related burden of acrylamide. Acrylamide is a toxic substance classified by the International Agency of Research on Cancer, as well as the Deutsche Forschungsgemeinschaft, as a probable human carcinogen. METHODS: A venous blood sample was taken in order to determine the smoking-specific acrylnitrile adduct N-cyanoethylvaline and the acrylamide adduct N-2-carbamoylethylvaline in a female study population expecting delivery soon. A standardized questionnaire was used to determine the consumption of acrylamide-contaminated food. The results of our questionnaire were transferred to a linear evaluation system. Finally, anamnestic data of the questionnaire were correlated to objective parameters such as blood levels of hemoglobin adducts of acrylamide and acrylonitrile. RESULTS: A positive correlation between the acrylamide intake and the levels of hemoglobin adducts in our study population was not proven. CONCLUSIONS: Evaluation of food-related exposure to acrylamide is difficult due to several reasons. Firstly, the validity of anamnestic data strongly depends on the patient's ability to remember precisely all consumed food (quality as well as quantity) over a 3-month period. In addition, the contamination of acrylamide in food varies from one product to another; even the contamination of the same product is variable. Therefore, the missing correlation between the questionnaire and hemoglobin adduct rates is rather due to restricted validity of anamnestic data.

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PubMed2005

Change in content of sugars and free amino acids in potato tubers under short-term storage at low temperature and the effect on acrylamide level after frying.

Changes in the sugar and amino acid contents of potato tubers during short-term storage and the effect on the acrylamide level in chips after frying were investigated. The acrylamide content in chips began to increase after 3 days of storage at 2 degrees C in response to the increase of glucose and fructose contents in the tubers. There was strong correlation between the reducing sugar content and acrylamide level, R(2)=0.873 for fructose and R(2)=0.836 for glucose. The sucrose content had less correlation with the acrylamide content because of its decrease after 4 weeks of storage at 2 degrees C, while the reducing sugar in potato tubers and the acrylamide in chips continued to increase. The contents of the four amino acids, i.e., asparatic acid, asparagine, glutamic acid and glutamine, showed no significant correlation with the acrylamide level. These results suggest that the content of reducing sugars in potato tubers determined the degree of acrylamide formation in chips. The chip color, as evaluated by L* (lightness), was correlated well with the acrylamide content.

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PubMed2006

[Acrylamide content in potato crisps in Poland].

The main source of acrylamide in the diet are thermally processed carbohydrate-rich products, mainly those obtained from potatoes. Acrylamide is a substance with neurotoxic, genotoxic and carcinogenic properties. The International Agency for Research on Cancer classified it as a potential human carcinogen in 1994. The purpose of this study was to assess acrylamide content in 24 samples of crisps randomly collected in Poland in 2004. Acrylamide was determined in the form of brominated derivatives by gas chromatography coupled with mass spectrometry. The average acrylamide content in the crisp samples examined was 998 mg/kg of the product, ranging from 352 to 3647 microg/kg, depending on the type of the crisps. The factor determining the differences in acrylamide content in the product was also the manufacturer. The average content of acrylamide in the crisps produced by three different manufacturers (manufacturers 1-3) was ca. 600-900 microg/kg, and in the crisps produced by manufacturer 4 was ca. 3 times higher. Moreover, substantial differences were found between the same types of crisps produced by the same manufacturers but originating from different manufacturing batches. The results obtained suggest the effects of various technological processes and raw material types on the level of acrylamide in crisps.

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PubMedDate not supplied

Behavioral and pharmacological responses following acrylamide exposure in rats.

The onset of acrylamide related toxicity and indications of recovery were evaluated using several behavioral tasks. Rats were chronically housed and tested for the first 15 weeks of the study in running wheels where food and water consumption and activity were continuously monitored. Separate groups of animals were repeatedly tested on at least one additional behavioral task: an operant schedule FR20 GO/NO-GO, spontaneous and drug-induced locomotor activity, drug-induced asymmetric rotation, or splaying of the hindlimbs. Animals were administered acrylamide monomer in their drinking water (100 ppm) for a six week period. Behavioral evaluations were initiated up to six weeks prior to acrylamide exposure and continued up to 12 weeks after termination of the exposure. Operant behavior and spontaneous locomotor activity in an open field were not affected by acrylamide exposure. Nocturnal activity in running wheels was decreased, and hindlimb splay increased by exposure to acrylamide. Subsequent to injections of d-amphetamine locomotor activity in an "open field" was markedly increased following exposure to acrylamide. d-Amphetamine induced asymmetric rotation was also altered following acrylamide exposure. It is suggested that this altered pharmacological response was due to an effect of acrylamide on hepatic mechanisms or on central dopaminergic function.

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PubMed1984

Effects of acrylamide and some other sulfhydryl reagents on spontaneous and pathologically induced terminal sprouting from motor end-plates.

The innervation of the normal rat sternocostalis muscle exhibits a constant low level of short spontaneous terminal sprouts visible in zinc iodide-osmium (ZIO) and in methylene blue-stained preparations. Acrylamide inhibits these spontaneous sprouts in a dose-dependent manner. This inhibition is mimicked by N-ethylmaleimide (a sulfhydryl group blocking agent) and can be nullified when acrylamide is given after the sulfhydryl group protecting agent, dithiothreitol (DTT). This could not be reversed by giving DTT 3 hours after acrylamide. Furthermore, when given alone DTT increases the level of spontaneous terminal sprouting seen in ZIO and in methylene blue-stained preparations. These findings suggest that the binding of acrylamide to sulfhydryl groups is involved in the inhibitory process. Acrylamide also reduces the number and length of the reactionary terminal sprouts, seen in ZIO and in methylene blue-stained preparations, that follow partial denervation or local injection of botulinum toxin. These inhibitory effects are long-lasting; recovery still has not fully occurred 4 weeks after a single dose of acrylamide (50 mg/kg). The roles of glutathione and other sulfhydryl components of axons are discussed in relation to the mechanism of acrylamide neurotoxicity.

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PubMed1995

A lifetime oncogenicity study in rats with acrylamide.

A lifetime oncogenicity study in Fischer 344 rats was conducted to accurately characterize the carcinogenic potency of acrylamide. Acrylamide was administered in drinking water throughout the 106-week study at concentrations required to provide a dose of 0, 0.1, 0.5, or 2.0 mg/kg/day to males or 0, 1.0, or 3.0 mg/kg/day to females. Complete necropsy and gross pathology examinations were performed on all study animals. Histopathology examinations were conducted on selected tissues of all high-dose and control animals. Selected tissues from intermediate and low-dose groups were subjected to histopathological examinations as required to clarify high- and control-dose group observations. There was no visual observation of neurotoxicity in any study animal but sciatic nerve degeneration was observed in the male and female high-dose groups. Increased mortality related to acrylamide was observed in the high-dose male group from Month 17 to the end of the study and in the high-dose females during Month 24. Mesotheliomas of the testicular tunic were significantly increased in the high-dose male group. The combined incidence of mammary gland adenocarcinomas and fibroadenomas was significantly increased in both acrylamide-dosed female groups. Males and females in the high-dose groups as well as females of the low-dose group had significantly (p < 0.001) increased thyroid follicular cell adenomas and adenocarcinomas. A variety of other tumor types observed with increased incidence in a previous acrylamide oncogenicity study (i.e., combined CNS glial neoplasms, papillomas of the oral cavity, adenomas of the clitoral gland, and uterine adenocarcinomas) were not observed to be present at increased incidence in this study. This study confirms previously described acrylamide induction of benign tumors of the thyroid and mammary glands as well as mesotheliomas of the testis. By using a larger number of animals with an unbalanced study design, this study showed that acrylamide did not induce glial tumors and demonstrated that the no-observable-effect level for scrotal mesotheliomas is 0.5 mg/kg. It also demonstrated that the increased incidence of mammary tumors was again within historical control ranges.

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PubMed2005

The formation of acrylamide in UK cereal products.

Many bakery products sold in the UK such as crumpets, batch bread and Naan might be expected to show high levels of acrylamide because they have strong Maillard colours and flavours. However, analysis of commercial products has shown that the highest levels of acrylamide are seen in dry biscuit type products. With the exception of spiced products such as ginger cake, moist high sugar products (e.g. cakes and fruit loaves) show relatively low levels of acrylamide, even in darkly browned crusts. This is in contrast to bread where acrylamide levels in excess of 100 microg/kg are common in the crust region, but are diluted by low levels in the crumb. Acrylamide levels in bread are significantly raised by domestic toasting, but other products such as crumpets and Naan bread have been found to be less sensitive. A mathematical model has been developed (and validated against tests on model dough) which shows that once obvious recipe differences are allowed for, the key factor limiting acrylamide levels is crust moisture. Chemical decay of acrylamide and depletion of amino acids are also limiting factors at higher temperatures.

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PubMed1986

The axon reaction in spinal ganglion neurons of acrylamide-treated rats.

Rats were given acrylamide in doses of either 30 or 50 mg/kg (5 days each week) for up to 3 weeks and killed at weekly intervals. The right sciatic nerve was tied tightly at the level of the major trochanter 4 days before killing the animals by perfusion fixation when ipsilateral and contralateral sensory ganglia (L5 and L6) were removed. The effects on neuronal perikarya of axotomy alone, of acrylamide alone and of these combined were studied by light and electron microscopy. The responses to axotomy and to acrylamide intoxication shared certain features, namely peripheral Nissl substance and to a lesser degree nuclear eccentricity, nucleolemmal crenation and mitochondrial enlargement. Neurofilament loss was present only with acrylamide. In combined axotomy and acrylamide all these five features were prominent. These findings indicate firstly that the individual responses to axotomy and to acrylamide, while sharing several features, are subtly different and secondly that acrylamide appears to impede the vital neuronal responses directed towards repair of the axon.

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PubMed1990

Acrylamide impairs fast and slow axonal transport in rat optic system.

Effects of single and repeated doses of acrylamide on fast and slow axonal transport of radio labeled proteins following the injection of L-[4,5-3H] leucine have been studied in the optic system of male Sprague-Dawley rats. A single dose of acrylamide (100 mg/kg) had no effect, but higher concentrations (200-300 mg/kg) altered the distribution of fast axonally transported materials in optic nerves and optic tracts. Repeated doses of acrylamide (30 mg/kg/day, 5 days per week for 4 weeks) produced degeneration of tibial nerves but spared optic nerves and optic tracts. Fast axonal transport rate in optic axons was reduced by 50% (reduced to 4 mm/h from 8 mm/h) in acrylamide treated animals. Acrylamide also slowed the velocity of slow axonal transport of labeled proteins in optic axons to 1.0 mm per day from 1.3 mm per day. Since acrylamide impaired the rate of both fast and slow axonal transport in the absence of overt morphological damage, it can be concluded that deficit in axonal transport is an important factor in the pathogenesis of axonal degeneration in acrylamide neuropathy.

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PubMed1985

Action of acrylamide on selected enzymes of energy metabolism in denervated cat peripheral nerves.

The effect of acrylamide on selected glycolytic and citric acid cycle enzymes has been studied in denervated cat sciatic nerves in vitro and in vivo. The enzyme activity of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), neuron specific enolase (NSE), succinate dehydrogenase (SDH), and lactate dehydrogenase (LDH), has been examined in saline-perfused, desheathed and denervated peroneal (P) and tibial (T) nerves from cats treated with acrylamide (15 mg/kg/day, s.c.) or vehicle for 15 days. GAPDH activity in denervated P and T nerve stumps was 2.0- and 2.3-fold higher than normal P and T nerve values. GAPDH activity in Schwann cells in denervated P and T nerves of acrylamide-treated cats was markedly reduced (56% and 61% of untreated denervated nerves, respectively). LDH and SDH activities were unaffected by acrylamide and NSE activity was absent in denervated nerve stumps. Acrylamide (0.5 and 20 mM) inhibited GAPDH activity in denervated nerve homogenates by 67% and 29%, respectively. This study demonstrates that acrylamide inhibits GAPDH in Schwann cells. The significance of GAPDH inhibition by acrylamide in denervated nerves and its relation to distal axonopathy has been discussed.

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PubMed1988

Progressive deficits in retrograde axon transport precede degeneration of motor axons in acrylamide neuropathy.

Single injection of acrylamide (1.3 mmol/kg, i.p.) inhibited retrograde axon transport of [125I]tetanus toxin in hen sensory and motor axons. Retrograde axon transport deficits appeared within hours of dosing with acrylamide. The inhibitory effect of acrylamide on retrograde axon transport was transient since transport deficits were not detectable 35 h after dosing. Acrylamide impaired the retrograde movement but not the uptake of [125I]tetanus toxin in the axon. Multiple doses of acrylamide (0.42 mmol/kg, i.p.) induced progressive clinical signs of acrylamide neuropathy that correlated with increasing deficits in retrograde axon transport of [125I]tetanus toxin to ventral spinal cord. Deficits were also observed in sensory neurons but were not statistically significant. Accumulated decrements in retrograde axon transport may be the underlying cause of degeneration of motor axons in acrylamide neuropathy in fowl.

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PubMed1983

Enhancement of lipid peroxidation in rat liver on acute exposure to styrene and acrylamide a consequence of glutathione depletion.

Lipid peroxidation, glutathione level and activity of glutathione-S-transferase were studied in liver and brain of rats 4 and 3 h after a single i.p. administration of 0, 25, 75, 100 mg/kg acrylamide or 0, 50, 100, 200, 600 mg/kg styrene, respectively. In liver both acrylamide and styrene caused an increase in lipid peroxidation and decrease in glutathione contents and activity of glutathione-S-transferase in a dose dependent manner, while in brain only acrylamide produced a decrease in glutathione content. The decrease in glutathione content was not always associated with increase of lipid peroxidation. The enhancement of lipid peroxidation occurred only when glutathione contents were depleted to certain critical levels. No effect of acrylamide or styrene was seen on lipid peroxidation under in vitro conditions. The addition of glutathione in the incubation mixture significantly inhibited the rate of lipid peroxidation of liver homogenates of acrylamide and styrene treated animals. The results suggest that enhancement of lipid peroxidation in liver on exposure to acrylamide or styrene is a consequence of depletion of glutathione to certain critical levels. The inhibition of glutathione-S-transferase activity by acrylamide and styrene suggests that detoxication of these neurotoxic compounds could be suppressed following acute exposure.

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