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PubMed1992

Effect of acrylamide monomer on hepatic CYP1A1 monooxygenase induction in rainbow trout.

1. Rainbow trout hepatic microsomes were pre-incubated in vitro with 1 pM, 1 nM, and 1 microM acrylamide for 20 or 30 min and ethoxyresorufin-O-deethylase (EROD) was measured. In vitro pre-incubation did not produce a significant decrease in EROD catalytic activity. 2. The effects of 50 ppm acrylamide monomer on hepatic CYP1A1 mRNA and CYP1A1 isozyme steady state levels in rainbow trout were determined after 6, 10, and 14 days of exposure. 3. Acrylamide monomer produced a 35% increase, 51% decrease and 140% increase in CYP1A1 mRNA at 6, 10 and 14 days, respectively, while at the same time CYP1A1 isozyme levels were decreased 12%, 67%, and 62% and EROD activity was decreased 33%, 90%, and 86%, respectively. 4. This indicates that acrylamide treatment may result in either a change in the translation of CYP1A1 mRNA or an isozyme selective inactivation of CYP1A1 resulting in loss of CYP1A1 apoprotein. 5. The effect of acrylamide treatment on hepatic CYP1A1 induction was determined using 10 or 14 day treatment with 50 ppm acrylamide monomer in a flowthrough exposure and induction with beta-naphthoflavone (beta-NF; 100 mg/kg i.p.) for 1 or 4 days. 6. Acrylamide and 1-day beta-NF had no effect on CYP1A1 mRNA levels when compared to 1-day beta-NF treatment alone, but acrylamide and 4-day beta-NF resulted in a 74% decrease in CYP1A1 mRNA compared to 4-day beta-NF treatment alone.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1989

Overwork weakness in rats with acrylamide neuropathy.

Exercised rats have larger myelinated nerve fibers than sedentary rats and exercised rats with acrylamide neuropathy have smaller fibers than acrylamide-treated sedentary rats. These nerve fiber changes were the result of work hypertrophy and overwork atrophy, respectively. This study was designed to reassess morphologic changes in nerves after overwork was induced in rats with acrylamide neuropathy and to test the effects of rest before and after an overwork period in rats with acrylamide neuropathy. The 4-week-old rats divided into four groups of eight rats. Acrylamide was administered to three groups (Groups 2, 3, and 4) to induce subacute paralysis followed by gradual ameriolation. Group 3 was exercised for the first 5 weeks and was rested for the last 5 weeks. Group 4 was exercised for the last 5 weeks. The diameter distribution of myelinated fibers of the tibial and sural nerves was analyzed. The percentage of larger myelinated fibers was decreased in all acrylamide-treated groups. The average values of fiber diameters in Group 4 were significantly smaller than injected sedentary animals (Group 2) or those with rest (Group 3), whereas no significant difference was found between the latter groups. Axonal degeneration of teased fibers was assessed in the tibial and sural nerves. The percentage of axonal degenerated fibers in exercised animals (Group 4) was significantly higher than in the other acrylamide-injected groups (Groups 2 and 3). This study supports the concept that acrylamide neuropathy worsens with moderate intensity of running activities for a prolonged period and that recovery may occur if vigorous exercise is avoided.

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PubMed1993

Degradation of acrylamide by immobilized cells of a Pseudomonas sp. and Xanthomonas maltophilia.

Two bacterial isolates capable of utilizing acrylamide as the sole source of carbon and nitrogen were isolated from herbicide-contaminated soil samples and identified as Pseudomonas sp. and Xanthomonas maltophilia. Batch cultures of Pseudomonas sp. and X. maltophilia completely degraded 62.8 mM acrylamide to acrylic acid and ammonia in 24 and 48 h, respectively. Pseudomonas sp. and X. maltophilia, when immobilized in calcium alginate, markedly increased the rate of degradation of acrylamide over batch cultures. Cells of the isolates immobilized in calcium alginate degraded acrylamide to acrylic acid and ammonia in less than 6 h. Initial metabolism of acrylamide by immobilized cells of Pseudomonas sp. followed by inoculation with nonimmobilized cells after 6 h totally removed acrylamide and its metabolites in 72 h. A similar procedure with X. maltophilia resulted in the total metabolism of acrylamide in 96 h. An inducible, intracellular amidase was responsible for the hydrolysis of acrylamide to acrylic acid and ammonia. The specific activity of Pseudomonas sp. amidase was higher than the specific activity of X. maltophilia amidase.

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PubMed1992

Intermediate filaments and steroidogenesis in adrenal Y-1 cells: acrylamide stimulation of steroid production.

The possible role of intermediate filaments in steroidogenesis was investigated in Y-1 mouse adrenal tumor cells by treatment with acrylamide, which is thought to disrupt intermediate filaments without directly affecting microtubules or microfilaments. Treatment of cells with 5 mM acrylamide increases steroidogenesis after a lag period of 4-6 h and induces rounding of the cells at approximately the same time. The effect of acrylamide on steroidogenesis is not cAMP mediated and occurs before pregnenolone formation. DNA synthesis is inhibited, while protein synthesis is not. Acrylamide does not affect polymerization/depolymerization of microtubules in vitro. Acrylamide stimulation of steroidogenesis is additive with that produced by either colchicine or ACTH, implying that acrylamide, ACTH, and colchicine act at different rate-limiting steps in steroidogenesis. In addition, acrylamide stimulation is additive with that of forskolin. Pretreatment of cells with taxol, an agent that specifically promotes microtubule polymerization, decreases acrylamide-stimulated (as well as colchicine or ACTH-stimulated) steroidogenesis, implying that there must also be some shared elements in the stimulating pathways. We hypothesize that regulation of steroidogenesis in the Y-1 cell depends on 1) disruption of a vimentin or tubulin coat surrounding lipid droplets and 2) possible functional shortening of the distance between cholesterol droplets and the mitochondrion. However, because of interactions between cytoplasmic fibers, it is currently impossible to say whether interruption of any one of them is a direct or indirect stimulus of steroidogenesis.

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PubMed1984

Carcinogenic effects of acrylamide in Sencar and A/J mice.

Acrylamide structurally resembles vinyl carbamate, a proposed proximate carcinogenic form of ethyl carbamate. To test the hypothesis that acrylamide should possess carcinogenic properties, it was tested in the Salmonella-microsome assay for point mutation, as a skin tumor initiator in the Sencar mouse, and for its ability to induce lung adenomas in the A/J mouse. Acrylamide was found to be without activity as a mutagen in Salmonella strains TA 1535, TA 1537, TA 98, and TA 100 both in the presence and absence of rat liver microsomes using both the plate and liquid suspension assays. However, acrylamide was found to approximate ethyl carbamate in potency as a tumor initiator in the skin of the female Sencar mice. As with ethyl carbamate, acrylamide was more potent by systemic routes of administration relative to topical application. Acrylamide was also found to induce lung adenomas in male and female A/J mice using both the p.o. and i.p. routes of administration. Acrylamide was approximately one-seventh as potent as ethyl carbamate in the induction of lung adenomas. These data confirm the hypothesis that acrylamide possesses carcinogenic properties similar to ethyl carbamate.

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PubMed2002

Acrylamide disturbs the subcellular distribution of GABAA receptor in brain neurons.

Mechanisms underlying the action of acrylamide on neurons were studied by monitoring the expression of GABA(A) receptor (R) in cultured brain neurons derived from chicken embryos. In situ trypsinization of the neurons and 3H-flunitrazepam binding assay were employed to examine the subcellular distribution of GABA(A)R. A 3-h exposure of the cultured neurons to 10 mM of acrylamide raised reversibly the proportion of intracellular (trypsin-resistant) 3H-flunitrazepam binding sites by about 48% and decreased cell surface binding 24% from respective control values, without altering total cellular binding and the affinity of the ligand. Moreover, the acrylamide treatment induced more intense perikaryal immunostaining of GABA(A)R alpha subunit proteins than that in control neurons but did not change the total level of cellular alpha immunostain, in accordance with the binding data. In the cell bodies of acrylamide-treated neurons, the level of neurofilament-200 kDa proteins was similar to control, whereas the tubulin protein content was significantly lowered approximately 51% from control, as revealed by quantifying the immunostained cytoskeletal elements. In addition, electron microscopic observations found reductions in the numbers of microtubules and neurofilaments in the perikarya of acrylamide-treated neurons. As exhibited by the 3H-leucine and 3H-monosaccharide incorporation experiments, the exposure to acrylamide inhibited the rate of general protein synthesis in the culture by 21%, while the rate of glycosylation remained unaltered. Furthermore, in situ hybridization analysis showed that acrylamide did not modify the expression of GABA(A)R alpha subunit mRNAs. Taken together, these data suggest that acrylamide may downregulate the microtubular system and disintegrate neurofilaments, and thereby block the intracellular transport of GABA(A)R, resulting in the accumulation of intracellular receptors.

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PubMed2006

Relationship between acrylamide and thermal-processing indexes in commercial breakfast cereals: a survey of Spanish breakfast cereals.

Breakfast cereals are significant contributors to the daily intake of food-derived acrylamide in Western countries. Acrylamide was determined by LC-MS in 60 commercial breakfast cereals marketed in Spain. Several SPE cartridges were evaluated for clarification of the aqueous extract. LOQ was 62 microg/kg . Acrylamide content ranged from < 62-803 microg/kg (average 292 microg/kg , and median 258 microg/kg , with an estimated acrylamide intake from breakfast cereals of 2.68 microg acrylamide/person/day. According to the German concept of minimization, a signal value 450 microg/kg was calculated. Relationships among acrylamide and some parameters of the studied samples such as type of cereal, its physical form (puffed and flaked) or certain ingredients in the formulation (proteins and dietary fibre content) were also investigated. Wheat-based cereals contained significantly higher levels of acrylamide, as did samples with higher fibre or protein content. In addition, puffed breakfast cereals also contained significantly higher levels of acrylamide. There was no significant correlation between acrylamide levels and contents of 5-hydroxymethylfurfural, furosine or cereal browning.

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PubMed2006

Studies on acrylamide levels in roasting, storage and brewing of coffee.

The content of acrylamide in coffee reaches a peak early in the roasting process, reflecting occurrence of both formation and destruction of acrylamide during roasting. Levels of acrylamide in the fully roasted product are a small fraction of the peak reached earlier. Glucose and moisture in green coffee do not show a significant correlation with acrylamide in roasted coffee. Pre-roasting levels of asparagine show a correlation only in Arabica coffee. The main factors affecting the level of acrylamide in roasted coffee appear to be the Arabica/Robusta ratio, with Robusta giving higher levels; time and degree of roast, with both shorter and lighter roasting at the edges of the normal roasting range giving higher levels; storage condition and time, with clear reduction at ambient storage. This storage reduction of acrylamide followed second order reaction kinetics with an activation energy of 73 KJ/mole. The acrylamide in roasted coffee is largely extracted into the brew and stable within usual time of consumption. As these four main factors also substantially affect the sensorial characteristics of the brew, and as modifications of the process have to comply with the consumer-accepted boundaries of taste profiles, only small effects on the acrylamide level are expected to be achievable.

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PubMed2005

Biological effects of Maillard browning products that may affect acrylamide safety in food: biological effects of Maillard products.

The heat-induced reaction of amino groups of amino acids, peptides, and proteins with carbonyl groups of reducing sugars such as glucose results in the concurrent formation of so-called Maillard browning products and acrylamide. For this reason, reported studies of adverse biological effects of pure acrylamide may not always be directly relevant to acrylamide in processed food, which may contain Maillard and other biologically active products. These may either antagonize or potentiate the toxicity of acrylamide. To stimulate progress, this paper presents an overview of selected reported studies on the antiallergenic/allergenic, antibiotic, anticarcinogenic/carcinogenic antimutagenic/mutagenic, antioxidative/oxidative, clastogenic (chromosome-damaging), and cytotoxic activities of Maillard products, which may adversely or beneficially impact the toxicity of acrylamide. The evaluation of biological activities of Maillard products and of other biologically active food ingredients suggests that they could both enhance and/or ameliorate acrylamide toxicity, especially carcinogenicity, but less so neurological or reproductive manifestations. Future studies should be directed to differentiate the individual and combined toxicological relationships among acrylamide and the Maillard products, define individual and combined potencies, and develop means to prevent the formation of both acrylamide and the most toxic Maillard products. Such studies should lead to safer foods.

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PubMed2005

Kinetic models as a route to control acrylamide formation in food.

A kinetic model for the formation of acrylamide in potato, rye and wheat products has been derived, and kinetic parameters calculated for potato by multi-response modeling of reducing sugar (glucose and fructose), amino acid, asparagine and acrylamide concentrations with time. The kinetic mechanism shares, with Maillard browning, a rate limiting (probably dicarbonylic) intermediate, and includes reaction steps of this intermediate which are competitive with respect to acrylamide formation. A pathway representing physical and/or chemical losses of acrylamide accounts for the measured reduction of acrylamide yield at long reaction times. A mechanistic hypothesis regarding the competing reactions of Strecker aldehyde formation and tautomerization followed by beta-elimination to give acrylamide, features in the kinetic model and can be used to determine the factors which steer the reaction towards acrylamide. A predictive application of this model is for 'what-if' experiments to explore the conditions which lead to reduced acrylamide yields.

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PubMed2005

Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure.

Food is assumed to be one major source of acrylamide exposure in the general population. Acrylamide exposure is usually assessed by measuring hemoglobin adducts of acrylamide and its primary metabolite glycidamide as biomarkers. Little is known about the impact of acrylamide in food on biomarkers of acrylamide exposure. Therefore, CDC is conducting a feeding study to investigate the effect of consumption of endogenous acrylamide in food on biomarkers of acrylamide exposure. As part of this study, we performed a pilot study to obtain further information on the magnitude of the changes in biomarker levels after consumption of high amounts of potato chips (21 ounces) over a short period of time (1 week) in non-smokers. After 1 week, biomarkers levels increased up to 46% for acrylamide adducts and 79% for glycidamide adducts. The results indicate that changes in biomarker levels due to consumption of potato chips can be detected. However, because of the design of this pilot study, the observed magnitude of change cannot be. generalized and needs to be confirmed in the main study.

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PubMed2005

A new approach for the assessment of acrylamide toxicity using a green paramecium.

Exposure to acrylamide induces neurotoxic effects in humans. In addition, it induces genotoxic, reproductive and carcinogenic effects in laboratory animals. However, no convenient bioassay system for assessing acrylamide toxicity to animal and plant cells has been proposed to date. The present study aims to evaluate acrylamide toxicity to a green paramecium, Paramecium bursaria, bearing many endosymbiotic algae, because some chemicals are highly toxic to paramecia or microalgae, and some protozoa are already used for evaluation of environmental contaminations. Results showed that high acrylamide concentrations (> or = 1500 mg/l) have a lethal effect on P. bursaria. Although low acrylamide concentrations (< or = 150 mg/l) induced less change on the paramecium growth, the number of endosymbiotically growing algal cells drastically decreased. The acrylamide concentration required to induce a 50% decrease in the cell number (IC(50)) was determined to be 7.8 mg/l for endosymbiotic algae, indicating that the algal sensitivity to acrylamide was 7 and 15 times higher than that of Syrian hamster embryo (SHE) cells and the host cells, respectively. Here, we propose the use of P. bursaria being a convenient and sensitive bioindicator as a new approach for the assessment of acrylamide toxicity.

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PubMed2004

Extremely low dose of acrylamide decreases lifespan in Caenorhabditis elegans.

The neurotoxic, genotoxic and carcinogenic effects of industrial exposure to acrylamide have been studied in animals and humans for more than 30 years. A recent search for the cause of high background levels of acrylamide in industrially unexposed people revealed that it is formed during the frying or baking of foods by means of the Maillard reaction. To evaluate the biological consequences of continuous exposure to acrylamide at levels found in common foodstuffs, we studied the effects of acrylamide on the three parameters of (1) growth, (2) fecundity and (3) lifespan in the nematode Caenorhabditis elegans. As for growth and fecundity, no deleterious consequences were observed when the animals were raised in the acrylamide concentrations of 0.5 microg/L to 5mg/L, which are commonly found in daily consumed foodstuffs. Conversely, in 500 mg/L of acrylamide, they showed retarded growth with reduced body and brood sizes. Unlike the first two parameters, however, lifespan decreased significantly even in 0.5 microg/L of acrylamide, the maximum theoretical concentration allowed in drinking water by the WHO and US EPA. Very interestingly, the acrylamide effect on lifespan is biphasic as lifespan increased to near normalcy in 5 mg/L and decreased again in 500 mg/L.

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PubMed2000

Acrylamide-regulated neurofilament expression in rat pheochromocytoma cells.

Using the rat pheochromocytoma cell line (PC12), we present molecular evidence that the neurotoxicant acrylamide directly induces neurofilament gene expression, and the signaling pathways are initially distinctive from, but eventually merged into, that for nerve growth factor (NGF)-induced neurofilament expression. In PC12 cells, acrylamide increased neurofilament protein levels and synthesis. Acrylamide had no effect on the stability of neurofilament mRNAs suggesting that it directly increased neurofilament mRNA synthesis. K252a, a selective inhibitor for NGF receptor gp140trk, had no effect on acrylamide induction, but completely inhibited NGF-induced neurofilament protein synthesis. Therefore, the initial step for acrylamide signaling was distinctive from NGF. Dexamethasone reversed the effects of both NGF and acrylamide on neurofilament protein levels and synthesis indicated that there is a dexamethasone-sensitive signaling step upon which NGF and acrylamide merge, suggesting involvement of transcription-activating proteins like AP-1. These results, taken together with previous studies of transgenic mice that overexpress neurofilament genes, may partially explain the mechanisms of neurofilament accumulation in distal parts of large axons, a pathognomonic feature of acrylamide neurotoxicity in animals.

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PubMed2003

Investigations of factors that influence the acrylamide content of heated foodstuffs.

The acrylamide content of heated foodstuffs should be considered to be the net result of complex reactions leading to the formation and elimination/degradation of this compound. The present study, involving primarily homogenized potato heated in an oven, was designed to characterize parameters that influence these reactions, including the heating temperature, duration of heating, pH, and concentrations of various components. Higher temperature (200 degrees C) combined with prolonged heating times produced reduced levels of acrylamide, due to elimination/degradation processes. At certain concentrations the presence of asparagine or monosaccharides (in particular, fructose and also glucose and glyceraldehyde) was found to increase the net content of acrylamide. Addition of other free amino acids or a protein-rich food component strongly reduced the acrylamide content, probably by promoting competing reactions and/or covalently binding acrylamide formed. The dependence on pH of the acrylamide content exhibited a maximum around pH 8; in particular, lower pH was shown to enhance elimination and decelerate formation of acrylamide. In contrast, the effects of additions of antioxidants or peroxides on acrylamide content were small or nonexistent.

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PubMed2004

Reduction of acrylamide uptake by dietary proteins in a caco-2 gut model.

The report of elevated acrylamide levels in some foods raised an international health alarm, because acrylamide probably has carcinogenic, neurotoxic, and genotoxic properties. However, data on the bioavailability of acrylamide from food matrices in humans are limited. In particular, only little is known about the interactions of acrylamide with food ingredients. Using a human intestine model (Caco-2 cells), this study shows that acrylamide monomers are highly bioavailable and pass the cell monolayer via passive diffusion. Furthermore, acrylamide binds to dietary proteins such as chicken egg albumin under intestinal and cooking conditions. This binding reduces the concentration of acrylamide monomers and leads to a reduced uptake by Caco-2 cells. Hence, it is concluded that a protein-rich diet may reduce acrylamide uptake.

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PubMed2004

Influence of processing parameters on acrylamide formation during frying of potatoes.

Consistent evidence suggests that the probable human carcinogen acrylamide is formed in starch-rich foodstuffs through heat-induced interaction of asparagine and reducing sugars during Maillard browning. However, information regarding the influence of processing parameters on acrylamide formation is scarce. We investigated the impact of temperature, heating time, browning level, and surface-to-volume ratio (SVR) on acrylamide generation in fried potatoes. Acrylamide content was determined by liquid chromatography (LC) and electrospray ionization tandem mass spectrometry (ESI-MS/MS). In potato shapes with low SVR, acrylamide content consistently increased with increasing temperature and processing times. By contrast, in shapes with intermediate to high SVR, maximal acrylamide formation occurred at 160-180 degrees C, while higher temperatures or prolonged processing times caused a decrease of acrylamide levels. Moreover, browning levels were not a reliable measure of acrylamide content in large-surface products.

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PubMed2003

Dietary acrylamide and cancer of the large bowel, kidney, and bladder: absence of an association in a population-based study in Sweden.

Recently, disturbingly high levels of acrylamide were unexpectedly detected in widely consumed food items, notably French fries, potato crisps, and bread. Much international public concern arose since acrylamide has been classified as a probable carcinogen, although based chiefly on laboratory evidence; informative human data are largely lacking. We reanalysed a population-based Swedish case-control study encompassing cases with cancer of the large bowel (N=591), bladder (N=263) and kidney (N=133), and 538 healthy controls, assessing dietary acrylamide by linking extensive food frequency data with acrylamide levels in certain food items recorded by the Swedish National Food Administration. Unconditional logistic regression was used to estimate odds ratios, adjusting for potential confounders. We found consistently a lack of an excess risk, or any convincing trend, of cancer of the bowel, bladder, or kidney in high consumers of 14 different food items with a high (range 300-1200 microg kg(-1)) or moderate (range 30-299 microg kg(-1)) acrylamide content. Likewise, when we analysed quartiles of known dietary acrylamide intake, no association was found with cancer of the bladder or kidney. Unexpectedly, an inverse trend was found for large bowel cancer (P for trend 0.01) with a 40% reduced risk in the highest compared to lowest quartile. We found reassuring evidence that dietary exposure to acrylamide in amounts typically ingested by Swedish adults in certain foods has no measurable impact on risk of three major types of cancer. It should be noted, however, that relation of risk to the acrylamide content of all foods could not be studied.

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