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PubMed2003

Proton transfer reaction mass spectrometry, a tool for on-line monitoring of acrylamide formation in the headspace of maillard reaction systems and processed food.

The formation of acrylamide was measured in real time during thermal treatment (120-170 degrees C) of potato as well as in Maillard model systems composed of asparagine and reducing sugars, such as fructose and glucose. This was achieved by on-line monitoring of acrylamide released into the headspace of the samples using proton transfer reaction mass spectrometry (PTR-MS). Unambiguous identification of acrylamide by PTR-MS was accomplished by gas chromatography coupled simultaneously to electron-impact MS and PTR-MS. The PTR-MS ion signal at m/z 72 was shown to be exclusively due to protonated acrylamide obtained without fragmentation. In model Maillard systems, the formation of acrylamide from asparagine was favored with increasing temperature and preferably in the presence of fructose. Maximum signal intensities in the headspace were obtained after approximately 2 min at 170 degrees C, whereas 6-7 min was required at 150 degrees C. Similarly, the level of acrylamide released into the headspace during thermal treatment of potato was positively correlated to temperature.

Journal Article↗

PubMed1988

Acrylamide treatment of PtK1 cells causes dephosphorylation of keratin polypeptides.

Treatment of PtKl cells with 5 mM acrylamide for 4 hr results in alterations in the distribution of keratin filaments within the cells. This effect is reversible within 18 hr. Labeling of PtKl cells with 32P demonstrates that there are four phosphorylated keratins, having Mr of 56 k, 53 k, 45 k, and 40 k. Phosphate associated with these polypeptides appears to turn over with a t1/2 of 12 hr. Incubation of labeled cells in 5 mM acrylamide results in approximately 50% dephosphorylation of keratins within 2 hr, which is 3 times faster than normal turnover. Recovery of cells from acrylamide is accompanied by rephosphorylation of keratins within 18 hr. Analysis by 31P NMR spectroscopy shows that acrylamide treatments are accompanied by a transient decrease in soluble inorganic phosphate. This is followed by a rapid increase in Pi which gradually returns to normal levels. These studies show a strong correlation between phosphorylation of PtKl cell keratins and morphological response of keratin filaments to acrylamide. These observations suggest that normal distribution of keratin filaments may be, in part, mediated by protein phosphorylation.

Acrylamide↗

PubMed1984

The influence of systemic factors on acrylamide-induced changes in brain, nerve, and other tissues.

In order to define the locus of acrylamide neurotoxicity, the effects of chronic intoxication (total dose 500 mg/kg) on cholinergic synthesis and transport, the Schwann cell-myelin complex, lysosomal activity, and several metabolic pathways were determined in rat sciatic nerve, spinal cord, and brain. No changes were found in hematological measures or in the levels of clinically important blood enzymes, indicating no major damage to other organs. The activities of choline acetyltransferase (ChAT), 2',3'-cyclic nucleotide phosphohydrolase, beta-glucuronidase, and lactate dehydrogenase were unaffected in acrylamide paralyzed animals, but creatine kinase (CK) decreased in sciatic nerve, muscle, and brain, particularly in animals dying of the intoxication. CK blood and the CK isoenzyme patterns in blood were unchanged. The synthesis of protein in brain and spinal cord (measured in vivo) were decreased in rats exposed to high-dose acrylamide. However, in brain and cord, CK decreased only after animals became systemically ill and suffered weight loss, with the lowest activities in those animals sick enough to die. The degree of stress to which the animals had been subjected was indicated by enlargement of the adrenal glands and decreased sulfolipid synthesis in the adrenals. Rats exposed to 25 mg/kg/day acrylamide to a total dose of 250 mg/kg developed leg weakness but not paralysis or weight loss and had a 25% decrease in CK only in the distal sciatic nerve. Because of the apparently stress-related or agonal loss of CK, no specific effect of acrylamide on the enzyme could be definitely demonstrated. Neither could the changes in protein synthesis be attributed solely to a direct effect of the toxin. These results illustrate the difficulties encountered in interpreting intoxication studies that produce systemic illness and support the suggestion that CK activity may be a useful marker of the severity and duration of the agonal state in studies of postmortem human brain.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗

PubMed1995

The reproductive and neural toxicities of acrylamide and three analogues in Swiss mice, evaluated using the continuous breeding protocol.

Acrylamide is a known genetic, reproductive, and neural toxicant, although it is not known if one effect is predominant. The toxicities of several structural analogues of acrylamide have been incompletely characterized, and the relative sensitivity of the second generation is not known. The present studies were designed to explore the relationship between neurotoxicity and reproductive toxicity, to further characterize the toxicities of three acrylamide analogues, and to evaluate the relative sensitivity of a second generation to these compounds. For the F0 generation, male and female Swiss CD-1 mice were provided drinking water containing acrylamide (ACR; 3, 10, 30 ppm), N,N'-methylenebisacrylamide (MBA; 10, 30, 60 ppm), N-(hydroxymethyl)acrylamide (HMA; 60, 180, 360 ppm), or methacrylamide (MACR; 24, 80, 240 ppm) during and after a 14-week cohabitation. The last litter was reared and dosed after weaning until mating at 74 +/- 10 days of age with the same level of compound given to the parents Neurotoxicity was assessed at several times in both generations by measuring forelimb and hindlimb grip strength. In the F0 generation, ACR caused an 11% decrease in pup number without measurable neurotoxicity; female fertility was not affected. Although both generations consumed the same amount of ACR, there were larger changes in the fertility-related endpoints in the F1 mice than in the F0's, with no concomitant change in organ weights or sperm parameters. In F0 mice, MBA reduced the number of live pups and their adjusted weight, with no neurotoxicity and no change in F0 female reproduction. MBA caused greater adverse effects in the second generation, concomitant with increased consumption. In the F0 generation, HMA caused the largest decrease in pup number during cohabitation (26%) together with a small effect on grip strength. Female reproduction was not affected. The second generation consumed more HMA and showed slightly greater toxic effects. In both generations, MACR was negative for both neurotoxicity and reproductive toxicity. Dominant-lethal studies showed that the fertility effects for ACR, MBA, and HMA could be explained by a male-mediated increase in postimplantation loss. These studies found that dominant lethality occurred without structural effects on the reproductive system in the presence of only minor effects on grip strength and without detectable neural histopathology. Female reproduction was not significantly affected by these compounds at the doses used. Thus, these data confirm the male as the affected gender and that the reproductive toxicity was greater than motoneuron toxicity when measured as grip strength.

Acrylamide↗

PubMed2005

Quality related minimization of acrylamide formation--an integrated approach.

An integrated approach is described with respect to acrylamide minimization in heated foodstuffs. All relevant variables have to be considered and the main focus is on maintaining the expected product quality. The role of the processes at the interface between product and heating medium during processing is characterized for the case of frying operations. Examples of parameters influencing these processes with respect to minimizing acrylamide and maintaining product quality (e.g. brown color) are described. First, the local distribution of acrylamide in a French fries type model food was investigated. Lowering water activity at the surface of French fries before frying contributes to a reduction of acrylamide without lowering product quality. Both pre-drying of the potato sticks before frying and an increasing of salt concentration at the product surface by coating with a salt solution showed positive effects. Additionally, it was demonstrated by simulation that combined effects of these measurements may enable a reduction of up to 80% in the acrylamide content.

Acrylamide↗

PubMed1983

Effect of acrylamide on neurotransmitter metabolism and neuropeptide levels in several brain regions and upon circulating hormones.

The effect of acute and subchronic acrylamide treatment on levels of dopamine, serotonin, and their metabolites was determined in several brain regions of the rat. Concentrations of several neuropeptides and circulating hormones were also measured. Both a single and repeated doses of acrylamide resulted in elevated levels of 5-hydroxyindolacetic acid in all regions studied (frontal cortex, striatum, hippocampus, brain stem, and hypothalamus). Changes in regional content of other monoamines were much less pronounced. Turnover studies following pargyline blockage of monoamine oxidase, suggested results were due to increased rates of serotonin turnover in acrylamide-treated rats. Changes in neuropeptide levels were only detected in the hypothalamus where a single acrylamide treatment caused elevated levels of beta-endorphin and substance P, and in frontal cortex where met-enkephalin levels were higher after repeated acrylamide injection. Such repeated injection caused a major depression in plasma levels of testosterone and prolactin.

Acrylamide↗

PubMed1996

A possible tertiary structure change induced by acrylamide in the DNA-binding domain of the Tn10-encoded Tet repressor. A fluorescence study.

A thorough investigation of the acrylamide fluorescence quenching of F75TetR, a mutant of the Tn10-encoded TetR repressor containing a single Trp residue at position 43, was carried out. The Trp-43 residue is located in a helix alpha-turn-helix alpha (H-t-H) motif involved in the specific binding of F75TetR to the operator site in specific DNA. Distinct Ranges of acrylamide concentration have been assumed. At acrylamide concentrations below 0.15-0.2 M (a usual range of values in fluorescence quenching studies) the observed limited tertiary structure change induced by acrylamide is consistent with a noncooperative local unfolding of the DNA-binding domain. It is suggested that penetration of the neutral quencher could cause the deletion of a hydrophobic tertiary structure contact, partly involving TrP-43, responsible for the anchoring of the H-t-H motif inside the three-helix protein bundle, characterizing the N-terminal part. Correspondingly, the affinity of the mutant repressor for the operator was shown to decrease substantially (about five orders of magnitude), seemingly losing its specificity. A subsequent phase, up to 0.8 M acrylamide, was observed in which the involved intermediate protein structure is not further perturbed, nor is DNA binding.

Acrylamide↗

PubMed1986

Monitoring exposure to acrylamide by the determination of S-(2-carboxyethyl)cysteine in hydrolyzed hemoglobin by gas chromatography-mass spectrometry.

Acrylamide is a potent cumulative neurotoxin in animals and man. In vivo exposure to this electrophile results in the formation of a covalently bound reaction product with cysteine residues in hemoglobin. This adduct yields on acid hydrolysis S-(2-carboxyethyl)cysteine which has been analyzed by capillary gas chromatography with mass spectrometry. Globin isolated from the blood of rats exposed to acrylamide was spiked with an internal standard (globin treated in vitro with d3-acrylamide) and was then hydrolyzed with 6 N HCl. The protein hydrolysate was fractionated on a Dowex 50W H+ ion exchange column and the amino acids in the partially purified extract were determined as N-heptafluorobutyryl methyl esters using an OV-1701 fused silica capillary column. Quantitation was made by chemical ionization (isobutane) selective ion monitoring in which the ions m/z 386 (M-OCH3)+ derived from derivatized S-(2-carboxyethyl)cysteine in the sample and the corresponding ion m/z 389 from the added deuterium-labeled internal standard were monitored. The dose-response relationship between production of hemoglobin adduct and dose of acrylamide (0.1 mg/kg-5 mg/kg) is curved, showing an increasing slope with increasing doses of acrylamide.

Acrylamide↗

PubMed1986

Altered phosphorylation of rat neuronal cytoskeletal proteins in acrylamide induced neuropathy.

The activity of protein kinase has been assayed in neurofilament preparations from spinal cords of rats treated with acrylamide. Animals received 50 mg/kg, i.p., of acrylamide per day for a total of 5 or 10 days; these doses produce mild and marked symptoms of neurological damage, respectively. Incorporation of phosphate into proteins was determined using [gamma-32P]ATP followed by SDS-PAGE. Total phosphorylation of neurofilament preparations was significantly increased only in the animals treated with the 500 mg/kg cumulative dose of acrylamide. Phosphorylation of the 200 and 155 kdalton subunits of the neurofilaments was increased by 20-40% in the acrylamide treated groups. The phosphorylation of the 70 kdalton neurofilament subunit was unchanged in the 250 mg/kg group and was significantly decreased in the 500 mg/kg group. Phosphorylation of other protein bands was not altered. These results suggest a mechanism by which acrylamide might produce axonal neurofilamentous accumulations.

Acrylamide↗

PubMed1995

Acrylamide: a review of its genotoxicity and an assessment of heritable genetic risk.

An updated review of the genotoxicity studies with acrylamide is provided. Then, using data from the studies generating quantitative information concerning heritability of genetic effects, an assessment of the heritable genetic risk presented by acrylamide is presented. The review offers a discussion of the reactions and possible mechanisms of genotoxic action by acrylamide and its epoxide metabolite glycidamide. Several genetic risk approaches are discussed, including the parallelogram, direct (actually a modified direct), and doubling dose approaches. Using data from the specific-locus and heritable translocation assays, the modified direct and doubling dose approaches are utilized to quantitate genetic risk. Exposures of male parents to acrylamide via inhalation, ingestion, and dermal routes are also quantitated. With these approaches and measurements and their underlying assumptions concerning extrapolation factors (including germ cell stage specificity, DNA repair variability, locus specificity), number of human loci associated with dominant disease alleles, and spontaneous mutation rates, an assessment of heritable genetic risk for humans is calculated for the three exposure scenarios. The calculated estimates for offspring from fathers exposed to acrylamide via drinking water are up to three offspring potentially affected with induced genetic disease per 10(8) offspring. Estimates for inhalation or dermal exposures suggest higher risks for induced genetic disease in offspring from fathers exposed in occupational settings.

Acrylamide↗

PubMed1989

Breathing pattern, lung inflation reflex and airway tone in acrylamide neuropathy.

Slowly adapting pulmonary stretch receptors (SARs) participate in numerous respiratory reflexes, including the Hering-Breuer lung inflation reflex (HBR), and reflex control of respiratory rate and depth. In addition, SAR discharge may modulate airway tone. We studied the effect of acrylamide neuropathy, which causes reversible dysfunction of SARs and their myelinated vagal afferents, on the breathing pattern, HBR and airway tone in conscious dogs. As neuropathy evolved, breathing became slow and deep, and both the apnoeic and bronchodilatory responses to lung inflation were markedly reduced, findings consistent with SAR dysfunction. Recovery of clinical neuropathy and respiratory reflexes followed acrylamide withdrawal. Despite the obvious abnormalities of SAR-mediated reflexes in acrylamide-affected dogs, airway tone remained normal and sinus arrhythmia prominent in the presence of neuropathy, suggesting that small diameter vagomotor efferents are relatively resistant to acrylamide. Acrylamide neuropathy provides a useful preparation for the study of vagomotor function in animals in which feedback from myelinated pulmonary afferents is attenuated.

Acrylamide↗

PubMed1989

Cytoskeletal effects of acrylamide and 2,5-hexanedione: selective aggregation of vimentin filaments.

Several neurotoxic compounds cause aggregation of neurofilaments in peripheral axons. This may represent a primary action of these chemicals or a secondary response to other cellular damage. To distinguish between these possibilities, the effects of acrylamide and 2,5-hexanedione (2,5-HD) on vimentin were examined in PtK2 cultured cells. Vimentin intermediate filaments were chosen because they are closely related, in structure, to neurofilaments. Effects on other components of the cytoskeleton (cytokeratin filaments, microtubules, and microfilaments) were also determined. Both acrylamide and 2,5-HD caused aggregation of vimentin filaments in a concentration-dependent fashion; these effects occurred at a lower concentration than alterations in other cytoskeletal filaments. The effects of both acrylamide and 2,5-HD were reversible, except at high concentrations of 2,5-HD. Crosslinking of cytoskeletal proteins was also examined. High-molecular-weight proteins with vimentin-like immunoreactivity were detected on blots from cells exposed to high concentrations of 2,5-HD. No crosslinked protein was detected after acrylamide treatment. These results suggest that both acrylamide and 2,5-HD cause a primary collapse of vimentin intermediate filaments in cultured cells. The initial redistribution of vimentin filaments occurred without apparent crosslinking of cytoskeletal proteins. The aggregation of vimentin filaments in cultured cells and of neurofilaments in vivo may share a common molecular mechanism.

Acrylamide↗

PubMed1993

Acrylamide as an inducer of metabolic activation system (S9) in rats.

The S9 fraction was prepared from rats i.p. injected with a single dose of 75 mg/kg acrylamide. The efficiency of the acrylamide induction procedure was verified on Salmonella mutagenicity testing (TA98 and TA100) using a number of known mutagens. These mutagens are aflatoxin B1, benzo[alpha]pyrene, 2-acetylaminofluorene and sodium azide. The activity of the mutagen is measured in terms of histidine revertant numbers which were found to be almost proportional to the concentration of acrylamide-induced S9. The maximum activation of the mutagens (except sodium azide) was recorded using around 50 microliters of S9 per plate. The efficiency of our prepared S9 fraction as a metabolic activator for some known mutagens is comparable to that of standard S9. On the basis of our results, acrylamide-induced S9 demonstrated considerable increase in the activation of the tested compounds. Accordingly, acrylamide could be used as an additional procedure for the induction of rat hepatic enzymes (S9).

2-Acetylaminofluorene↗

PubMed1996

Acrylamide-induced neuropathic changes in rat enteric nerves: similarities with effects of streptozotocin-diabetes.

The effect of acrylamide intoxication (a widely used model for autonomic neuropathy) on the fluorescence intensity and density of catecholamine- and peptide-containing nerve fibres and tissue content of noradrenaline and the peptides vasoactive intestinal polypeptide, calcitonin gene-related peptide, substance P and neuropeptide Y in the enteric nerves of rat ileum was examined. Histochemical and immunohistochemical techniques were used to localize catecholamine- and peptide-containing nerve fibres. The tissue content of noradrenaline was measured using high-performance liquid chromatography, and an enzyme-linked immunosorbent assay technique was used to determine the tissue content of the peptides investigated. Acrylamide intoxication caused a significant decrease in the density of catecholamine-containing nerve fibres and tissue content of noradrenaline in the myenteric plexus of rat ileum. A decrease in tissue content and immunoreactivity of calcitonin gene-related peptide and an increase in vasoactive intestinal polypeptide was seen in the myenteric plexus of ileum from acrylamide-intoxicated rats. In the submucous plexus, the acrylamide treatment caused a decrease in calcitonin gene-related peptide immunoreactivity and an increase in vasoactive intestinal polypeptide and neuropeptide Y immunoreactivity. There was no change in either tissue content or immunoreactivity of substance P in both myenteric and submucous plexuses of the treated rat ileum. These changes have a striking similarity with those found in the enteric nerves of streptozotocin-diabetic rat ileum, suggesting the possible presence of an underlying common mechanism(s) in the development of neuropathic changes in the autonomic nerves of acrylamide-intoxicated and streptozotocin-diabetic rats.

Acrylamide↗

PubMed1994

Acrylamide increases in vitro calcium and calmodulin-dependent kinase-mediated phosphorylation of rat brain and spinal cord neurofilament proteins.

Male Sprague-Dawley rats were administered a daily i.p. dose of 0.70 mmol/kg body weight of acrylamide, propionamide (a non-neurotoxic structural analog of acrylamide) or deionized water. Animals were sacrificed when signs of severe neurotoxicity were apparent. Neurofilaments (NFs) and endogenous kinase were isolated from the brain and spinal cord by axonal floatation. Increased in vitro Ca2+/calmodulin-dependent phosphorylation of endogenous and exogenous NF proteins and autophosphorylation of Ca2+/calmodulin protein kinase II (CaM kinase II, EC 2-7-1-37) were observed in samples from both brain and spinal cord of acrylamide-treated animals compared with controls. There was no significant difference between samples isolated from propionamide-treated animals and controls. Increased calmodulin binding to brain supernatant CaM kinase II was also observed as a result of acrylamide treatment. There was no significant difference observed in the amount of antibody binding to the alpha-subunit of brain supernatant CaM kinase II between treated or control animals. These results suggest that increased CaM kinase II-dependent phosphorylation of cytoskeletal proteins may be involved in the mechanisms of acrylamide-induced neurotoxicity.

Acrylamide↗

PubMed1987

Comparative tissue distribution and excretion of [1-14C]acrylamide in beagle dogs and miniature pigs.

Male beagle dogs and miniature pigs were given acrylamide in the diet for 3-4 wk at a dosage of 1 mg/kg/day. They were then given [1-14C]acrylamide as a single oral dose of 1 mg/kg. The animals were killed 6 hr or 1, 2, 4 or 14 days after administration of the radioactive compound and tissues were analysed for radioactivity. The radiolabelled material was distributed to a major extent in muscle tissue in both species (31-35% of the dose at 6 hr and 5-7% at 14 days). Although the nervous system is the primary target for acrylamide monomer toxicity, less than 1% of the administered 14C was found in the brain in both species. No neurotoxic signs were evident during the exposure period at the dosage used. Analysis of discrete areas of the brain for radioactivity revealed that the levels of penetration of [1-14C]acrylamide in brain paralleled the vascularization pattern of the tissues. Approximately 60% of the administered radiolabel was excreted in the urine in both species and smaller amounts were excreted in the faeces. However, recovery in the faeces was higher in pigs (c. 25%) than in dogs (c. 7%) and this and the considerably higher levels demonstrated in the gastro-intestinal tract of the pigs indicated that the absorption of acrylamide was more rapid and more extensive in dogs than in pigs.

Acrylamide↗

PubMed2005

Determination of acrylamide and methacrylamide by normal phase high performance liquid chromatography and UV detection.

A method using normal phase high performance liquid chromatography (NP-HPLC) with UV detection was developed for the analysis of acrylamide and methacrylamide. The method relies on the chromatographic separation of these analytes on a polar HPLC column designed for the separation of organic acids. Identification of acrylamide and methacrylamide is approached dually, that is directly in their protonated forms and as their hydrolysis products acrylic and methacrylic acid respectively, for confirmation. Detection and quantification is performed at 200 nm. The method is simple allowing for clear resolution of the target peaks from any interfering substances. Detection limits of 10 microg L(-1) were obtained for both analytes with the inter- and intra-day RSD for standard analysis lying below 1.0%. Use of acetonitrile in the elution solvent lowers detection limits and retention times, without impairing resolution of peaks. The method was applied for the determination of acrylamide and methacrylamide in spiked food samples without native acrylamide yielding recoveries between 95 and 103%. Finally, commercial samples of french and roasted fries, cookies, cocoa and coffee were analyzed to assess applicability of the method towards acrylamide, giving results similar with those reported in the literature.

Acrylamide↗

PubMedDate not supplied

Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation.

Acrylamide is an important industrial chemical which is neurotoxic to experimental animals as well as humans and recently has been shown to be mutagenic and carcinogenic. Despite much research it is still unclear whether the parent compound or a metabolite is responsible for the observed toxic effects. Contradictory results as to the role of cytochrome P-450 mediated metabolism of acrylamide in the induction of neurotoxic effects prompted us to investigate the possible formation of glycidamide, a reactive epoxide metabolite. The formation of this epoxide was strongly indicated by the identification by means of gas chromatography-mass spectrometry of derivatized S-(2-carboxy-2-hydroxyethyl)cysteine in hydrolyzed hemoglobin samples from rats treated with acrylamide in vivo and in microsomal suspensions of acrylamide with cysteine in vitro. This amino acid was found to be present in uninduced and phenobarbital-induced Sprague-Dawley rats and absent in controls, but occurred in lower amounts than the adduct derived from the parent compound, S-(2-carboxyethyl)cysteine. This finding suggests that the possible role of glycidamide in the neurotoxicity and carcinogenicity of acrylamide should be evaluated further.

Acrylamide↗