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PubMed1994

Changes in Na-K ATPase and protein kinase C activities in peripheral nerve of acrylamide-treated rats.

In previous studies on rat peripheral nerve, we showed that acrylamide (ACR) exposure was associated with alterations in axonal and Schwann cell elemental composition that were consistent with decreased Na-K ATPase activity. In the present corollary study, the effects of ACR exposure on Na-K ATPase activity were determined in sciatic and tibial nerves. Subacute ACR treatment (50 mg/kg/d x 10 d, ip) significantly (p < .05) decreased Na-K ATPase activity by 45% in sciatic nerve but did not affect this activity in tibial nerve. Subchronic ACR treatment (2.8 mM in drinking water for 30 d) significantly decreased (p < .05) Na-K ATPase activities by 19% and 35% in sciatic and tibial nerves, respectively. Na-K ATPase activity was not altered in sciatic nerve homogenates exposed to 1.0 mM ACR in vitro. Since protein kinase C (PKC) has been proposed to play a role in the modulation of membrane Na-K ATPase function, PKC activity was also measured in sciatic nerve homogenates and subcellular fractions prepared from control and ACR-treated rats. Regardless of the ACR treatment protocol, PKC activity was elevated in nerve cytosol, but not in a particulate fraction. The results of this study suggest that decreased Na-K ATPase activity is involved in ACR-induced perturbation of axoplasmic and Schwann cell elemental composition in rat peripheral nerves and that loss of activity is not due to direct chemical inhibition of the enzyme. The role of PKC in ACR neurotoxicity requires further elucidation.

Acrylamide↗
PubMed1997

Extruded micronuclei induced by colchicine or acrylamide contain mostly lagging chromosomes identified in paintbrush smears by minor and major mouse DNA probes.

In the mouse bone marrow micronucleus assay, it was studied whether micronuclei (MN) could be expelled from polychromatic erythrocytes (PCE) in a similar way to the main nucleus. To avoid the disrupting centrifugation step of the conventional bone marrow preparation procedure, the paintbrush technique was used in the present experiments. With May-Grunwald-Giemsa staining of paintbrush slides, 5 % of the colchicine (COL)-induced MN were found attached to the outside membranes of PCE and were regarded as extruded. Of the acrylamide (AA)-induced MN, 22% were extruded. After fluorescence in situ hybridization (FISH) of a total of 300 MN per chemical treatment with the mouse minor and major satellite DNA probes, 9.7% MN were extruded in the COL group and 8.3% MN were extruded in the AA group. FISH showed that 76% of the retained COL-induced MN were signal-positive, indicating that they contained entire chromosomes. With AA, 29% minor-positive and 28.3 % major-positive retained MN were found, confirming its known clastogenicity. However, the observed frequency of signal-positive MN (1.7 MNPCE(pos)/ 1000 PCE) in the AA group was about three times higher than in the control (0.5 MNPCE(pos)/1000 PCE) which indicates that AA has aneugenic potential. FISH analysis of the extruded MN showed 72-100% major as well as minor signals. It is concluded that expelled MN contain mostly entire chromosomes.

Acrylamide↗
PubMed1987

Comparison of the dominant lethal effects of acrylonitrile and acrylamide in male Fischer 344 rats.

Acrylonitrile (ACN) and acrylamide (AA), structurally similar vinyl monomers, are both animal carcinogens. ACN is weakly mutagenic in bacteria and induces sister-chromatid exchange, unscheduled DNA synthesis and cell transformation in cells in culture. AA induces chromosomal aberrations in bone marrow, blood and germ cells in vivo, and dominant lethal mutations in the germ cells of male mice and rats. In the current study, the ability of AA and ACN to induce dominant lethal mutations in the germ cells of male Fischer 344 rats was compared. Three groups of 50 males were gavaged daily for 5 days with ACN (60 mg/kg in normal saline), AA (30 mg/kg in normal saline) or vehicle only; an additional group of 20 males received a single i.p. injection of 0.2 mg/kg triethylenemelamine (TEM) on the afternoon of day 5. Starting 1 day after exposure, each male was bred to one female per week for 4 weeks (TEM-exposed group) or 10 weeks (ACN, AA and control groups). Mating rates were reduced only during week 1 in the TEM-treated group; pregnancy rates were reduced only during week 2 in the AA-exposed group and week 4 in the TEM-treated group. Females were necropsied 13 days after the end of the appropriate mating week and the amount of pre- and post-implantation loss calculated. ACN treatment of male rats induced no increases in either pre- or post-implantation loss in females in any of the 10 weeks post-exposure examined.(ABSTRACT TRUNCATED AT 250 WORDS)

Acrylamide↗
PubMed1988

Mutagenic activity of acrylamide in eukaryotic systems but not in bacteria.

The vinyl monomer acrylamide (AA) was studied for its activity in a range of genotoxicity tests, including the Salmonella/microsome test, the fluctuation test using Klebsiella pneumoniae, the test for gene mutations at the TK and HPRT loci in L5178Y mouse lymphoma cells, tests for chromosomal aberrations and SCEs in V79 Chinese hamster cells, the sex-linked recessive lethal (SLRL) and somatic mutation and recombination (SMART) assays in Drosophila melanogaster and the mouse bone marrow micronucleus assay. AA showed genotoxic activity in most systems. The bacterial tests did not respond, in compliance with literature data; also in the Drosophila SLRL test, no significant increase in mutation rate was observed.

Acrylamide↗
PubMed1993

Acrylamide; induction of DNA damage, chromosomal aberrations and cell transformation without gene mutations.

The genotoxic potential of acrylamide monomer (AA), a compound familiar as a raw material of polyacrylamide electrophoresis gel, was extensively investigated in vitro. The results were clear cut: AA did not induce any gene mutations in Salmonella/microsome test systems (TA98, TA100, TA1535, TA1537), Escherichia coli/microsome assay (WP2 uvrA-) up to a dose of 50 mg AA/plate, or in HPRT-locus in Chinese hamster V79H3 cells (AA, 1-7 mM, 24 h treatment). On the other hand, AA showed a strong positive response: (a) in a Bacillus subtilis spore-rec assay (DNA damage) at 10-50 mg/disc, (b) to a chromosomal structural change test (AA, 2-5 mM, 24 h treatment), (c) to a polyploidy test (AA, 1-5 mM, 24 h treatment) in Chinese hamster V79H3 cells, (d) to a cell transformation assay in mouse BALB/c3T3 cells (AA, 1-2 mM, 72 h treatment). Sister chromatid exchange was also weakly but significantly induced by AA (AA, 1-2.5 mM, 24 h treatment) in Chinese hamster V79H3 cells. Carcinogenic potential of AA was reported in mice and rats several years ago. AA thus seems to be a typical clastogenic rodent carcinogen without any gene mutation potential. Furthermore, this experiment showed for the first time positive response of AA to a microbial test system (B. subtilis spore-rec assay).

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PubMed2003

Comparison of the hemoglobin adducts formed by administration of N-methylolacrylamide and acrylamide to rats.

Acrylamide (AM) and N-methylolacrylamide (NMA) are used in the formulation of grouting materials. AM undergoes metabolism to a reactive epoxide, glycidamide (GA). Both AM and GA react with hemoglobin to form adducts that can be related to exposure to AM. The objective of this study was to evaluate the extent to which NMA could form the same adducts as AM. N-(2-carbamoylethyl)valine (AAVal derived from AM) and N-(2-carbamoyl-2-hydroxyethyl)valine (GAVal derived from GA) were measured following a single oral dose of AM (50 mg/kg) or NMA (71 mg/kg) in male F344 rats. AAVal and GAVal were measured by a modified Edman degradation to produce phenylthiohydantoin derivatives and liquid chromatography/tandem mass spectrometry. In AM-treated rats, AAVal was 21 +/- 1.7-pmol/mg globin (mean +/- SD, n = 4), and GAVal was 7.9 +/- 0.8 pmol/mg. In NMA-treated rats, AAVal was 41 +/- 4.9 pmol/mg, and GAVal was 1.4 +/- 0.1 pmol/mg. Whether AAVal was derived from reaction of NMA with globin followed by loss of the hydroxymethyl group, or loss of the hydroxymethyl group to form AM prior to reaction with globin, is not known. However, the higher ratio of AAVal:GAVal in NMA-treated rats (29 vs. 2.6 in AM-treated rats) suggests that reaction of NMA with globin is the predominant route to AAVal in NMA-treated rats. The detection of GAVal in NMA-treated rats indicates oxidation of NMA, either directly or following conversion to AM. The lower levels of GAVal on NMA administration suggest that a much lower level of epoxide was formed than compared with AM treatment.

Acrylamide↗
PubMed1989

Axonal degeneration and axonal caliber alterations following combined beta,beta'-iminodipropionitrile (IDPN) and acrylamide administration.

A new model of neurofilamentous axonal abnormality is described which employs combined administration of beta,beta'-iminodipropionitrile (IDPN) and acrylamide (AC). The model was developed to test the hypothesis that IDPN-induced swelling increases the vulnerability of the distal axon to a second neurotoxic chemical insult. Rats were given a single intraperitoneal (IP) injection of IDPN (1.5 g/kg) one week before receiving a single injection of AC (75 mg/kg, IP). Axonal degeneration was observed at multiple levels along the sciatic nerve at two weeks (with reference to IDPN administration), and was not progressive up to five weeks. Quantitation of degenerating fibers demonstrated that the extent of degeneration increased distally along the sciatic nerve. Single administration of either IDPN or AC did not produce degeneration. Thus, IDPN-induced neurofilamentous swellings alter the susceptibility of the axon to AC neurotoxicity. Two variations of this model were also studied. First, rats given five daily injections of AC (30 mg/kg, IP) beginning one week following IDPN administration developed accumulations of fast axonally transported materials in IDPN-induced microtubule channels. Second, rats given chronic injections of AC (30 mg/kg, IP, five days/week, for four weeks), to reduce the delivery of neurofilaments to the proximal axon, developed less prominent axonal enlargements when challenged with IDPN. Thus, axonal atrophy can mask the development of neurofilamentous axonal swellings.

Acrylamide↗
PubMedDate not supplied

Ultrastructural changes in axons caused by acrylamide above a nerve ligature.

The ultrastructural features of the ascending degeneration produced by acrylamide in peripheral nerves above the point of nerve ligature have been described. Before the onset of signs of axonal degeneration abundant accumulation of smooth endoplasmic reticulum and vesicles occur particularly proximal to nodes of Ranvier, but also in internodal regions. Some mitochondrial accumulations occur distal to nodes of Ranvier. The changes closely resemble those found in axons up to 4 mm above a nerve crush in normal animals and appear to be essentially non-specific in nature. Their significance in relation to the subsequent axonal degeneration can only be guessed at.

Acrylamide↗
PubMedDate not supplied

Acrylamide-induced ascending degeneration of ligated peripheral nerve: effect of ligature location.

Acrylamide was administered to rats for 10 days (50 mg/kg/day) after ligation of either proximal (sciatic) or distal (posterior tibial) nerves. Morphologic evaluation of the nerves revealed severe degeneration 0.5 cm proximal to the ligature, with progressively less pronounced change at successively higher levels above the ligature, when compared with ligated non-treated controls. Although severe degeneration of the nerves was observed in both proximal- and distal-ligated groups of animals, the distal-ligated group showed slightly more change (at 0.5 cm above the ligature), suggesting a minor effect of distance of the site of nerve injury from the nerve cell body.

Acrylamide↗
PubMed1982

Acrylamide induces early morphologic reorganization of the neuronal cell body.

Rats were intoxicated with acrylamide monomer at 50 mg per kilogram per day; lumbar dorsal root ganglia and distal sural and tibial nerves were studied morphologically. At the sixth day of intoxication, large and small neuronal cell bodies showed a spectrum of remodeling changes that included nuclear eccentricity, cytoplasmic reorganization with an outer mantle of Nissl and an inner perinuclear zone of pigmented bodies, and increased perineuronal cells. Distal axons showed little degeneration at this time. These findings suggest that the cell body plays an important role in the pathogenesis of dying-back neurotoxic disease, and that there may be direct toxic affect on the perikaryon itself.

Acrylamide↗
PubMed1996

Nitrile hydratase and its application to industrial production of acrylamide.

Nitrile hydratase (NHase) was discovered in our laboratory. This enzyme was purified and characterized from various microorganisms. NHases are roughly classified into two groups according to the metal involved: Fe-type and Co-type. NHases are expected to have great potential as catalysts in organic chemical processing because they can convert nitriles to the corresponding higher-value amides under mild conditions. We have used microbial enzymes for the production of useful compounds: NHase has been used for the industrial production (production capacity: 30,000 tons/year) of acrylamide from acrylonitrile. This is the first successful example of a biotransformation process for the manufacture of a commodity chemical. This review summarizes the history of NHase studied not only from a basic standpoint but also from an applied point of view.

Acrylamide↗
PubMed1993

A nonlinear dosimetric model for hemoglobin adduct formation by the neurotoxic agent acrylamide and its genotoxic metabolite glycidamide.

Hemoglobin (Hb) adducts, formed by the neurotoxic agent acrylamide (AA) and its genotoxic metabolite glycidamide (GA), were measured in the rat by means of a method for simultaneous determination of the adducts formed to cysteine. A novel, nonlinear dosimetric model was developed to describe Hb adduct formation. This model incorporates the saturable kinetics of the metabolic conversion in vivo of AA to GA. The pharmacokinetic parameters Vmax and Km and the first-order rates of elimination, k1 and k2, for AA and GA from all processes except conversion of AA to GA, were estimated directly from Hb adduct data to 19 M hr-1, 66 microM, 0.21 hr-1, and 0.48 hr-1, respectively. At low concentrations, approximately 60% of AA was metabolized to GA. The nonlinear dosimetric model for adduct formation has potential general applicability in high-to-low-dose extrapolation of genotoxic effects.

Acrylamide↗
PubMed2001

New supports for enzyme immobilization based on copolymers of vinylene carbonate and acrylamide.

In this study, a series of beadlike and hydrophilic supports containing reactive cyclic carbonate groups for enzyme immobilization were prepared via reverse-phase suspension copolymerization of the aqueous solutions of vinylene carbonate (VCA), acrylamide (AA), and N,N'-methylene bisacrylamide in paraffin oil. The supports were used as a matrix for immobilization of trypsin and showed a considerable capacity to couple with trypsin and reasonable retention of activity for the immobilized trypsin, depending on the immobilization conditions, such as the content of VCA structural units, reaction time, and pH of the medium.

Acrylamide↗
PubMed1988

Quenching of tryptophan fluorescence in bovine lens proteins by acrylamide and iodide.

The microenvironments of tryptophan residues in bovine alpha-, beta H-, beta L and gamma-crystallins have been examined using acrylamide and KI quenching of fluorescence. From a consideration of the differential effects of the two quenchers, the quenching efficiencies and spectral changes, it was possible to distinguish tryptophans in different environments and to assign these to specific residues in the sequence. Two classes of tryptophan were identified in gamma-crystallin, one buried and one moderately accessible. The buried class contained tryptophans 42A and 125 which lie in the angles of the wedge-shaped domains of the protein. These residues, which had emission maxima at 326 nm, were not accessible to quenching by iodide. The more accessible residues, emitting at 334 nm, corresponded to tryptophans 64 and 148 which are in the widest part of the wedge-shaped subunit and close to the surface of the protein. The two beta-crystallins were virtually indistinguishable. They contained two buried tryptophans, probably residues 58 and 150, and three close to the surface, residues 81, 84 and 166. The quenching efficiencies for these two classes were lower than those observed with gamma-crystallin. Since the three-dimensional structures of the beta- and gamma-crystallins are probably very similar, this suggests that the polymeric nature of the beta-crystallins is responsible for the decreased accessibility of the tryptophans to the quenchers. alpha-crystallin demonstrated unusually high static quenching which made it difficult to distinguish different classes of tryptophan.(ABSTRACT TRUNCATED AT 250 WORDS)

Acrylamide↗
PubMed1994

Acrylamide induced immunosuppression in rats and its modulation by 6-MFA, an interferon inducer.

In the present communication, we describe acrylamide (ACR) induced immunotoxicity and its modulation by an interferon inducer, the 6th mycelial fraction acetone (6-MFA) of Aspergillus ochraceus ATCC 28706. ACR administration to rats produced a significant decrease in the weight of spleen (p < 0.001), thymus (p < 0.001) and mesenteric lymph nodes (p < 0.05). A decrease in cellularity of spleen (p < 0.001), thymus (p < 0.001), bone marrow (p < 0.001) and circulating blood lymphocyte population (p < 0.001) was also recorded. ACR suppressed the humoral as well as cell mediated immunity as assessed by erythrocyte antibody complement (EAC)-rosettes (p < 0.001), hemagglutination titre (p < 0.001), PFC (p < 0.001) and the delayed type hypersensitivity response against sheep red blood cells (SRBC, p < 0.001). ACR treated immunosuppressed rats when treated with 6-MFA restored the circulating lymphocyte number to the normal level and a partial recovery in the weight of spleen and thymus. Potentiation of EAC-rosettes, hemagglutination titre, IgM-PFC and DTH response against SRBC was observed. It is concluded that 6-MFA ameliorate the ACR induced toxicity. This study may be of significance in prevention of ACR toxicity.

Acrylamide↗
PubMed1997

Differential effects of acrylamide on the degeneration and regeneration of myelinated fibers between C57BL/Ola and C57BL/6J mice after crush injury.

To investigate differences in the pathologic processes between mutant C57BL/Ola (Ola) and normal C57BL/6J (6J) mice, the effect of acrylamide (ACR) on the degeneration and regeneration of myelinated fibers after crushing the sciatic nerve was morphometrically evaluated. Both Ola and 6J mice were treated with either ACR (subcutaneous injection of 50 mg/kg every other day for 13 days, n = 6) or physiological saline (n = 6). Morphometric evaluation of myelinated fibers of the sciatic nerve 5 mm distal to the proximal end of the crush site was performed systematically on day 14 of the crushing for each mouse. In Ola mice treated with either saline or ACR, large and small myelinated fibers remained without obvious progression of Wallerian degeneration, and degeneration of myelinated fibers was slower than in 6J mice. On the other hand, in 6J mice treated with either saline or ACR, many small myelinated fibers regenerated after degeneration and loss of both large and small myelinated fibers. In Ola mice, no statistically significant difference in the morphometric parameters was found between saline-treated and ACR-treated groups. Therefore, ACR did not have a significant effect on Wallerian degeneration of myelinated fibers in Ola mice. However, in 6J mice regenerated myelinated fibers were fewer in those receiving ACR than in those receiving saline. Therefore, ACR suppresses regeneration of myelinated fibers after crushing in 6J mice. A delay or partial failure of axonal sprouting and elongation may be responsible for the lower numbers of regenerated myelinated fibers. This study demonstrates the importance of the substrain differences in the degeneration and regeneration of myelinated fibers which may have implications for understanding the different susceptibilities to various neuropathies in man.

Acrylamide↗
PubMedDate not supplied

Linear versus nonlinear models for hemoglobin adduct formation by acrylamide and its metabolite glycidamide: implications for risk estimation.

Hemoglobin cysteine adduct levels formed by acrylamide (AA) and its epoxide metabolite glycidamide (GA) as previously determined (Bergmark et al., Toxicol. Appl. Pharmacol., 111: 352-363, 1991) in rats given single injections of AA were used to estimate tissue doses, D = integral of Cdt (area under the concentration curve in the blood compartment), of the two compounds. The data were adapted to linear or nonlinear kinetic models, where the latter model accounted for the Michaelis-Menten kinetics of the metabolic conversion of AA to GA. In the linear model, the first-order rates, k*, of elimination from all processes were estimated to be 0.50 and 0.48 h-1 for AA and GA, respectively. In the nonlinear model, the parametrical values Vmax = 19.1 h-1 and Km = 66 microM for the in vivo metabolic conversion of AA to GA, and k1 = 0.21 h-1 and k2 = 0.48 h-1 for the first-order rates of elimination from all other processes of AA and GA, respectively, were found to give the best fit to the exact dosimetric expressions [formula: see text] Using Equation B, it was estimated that the percentage of AA converted to GA approaches 58% when [AA]o, the initial concentration of AA, approaches zero. The implications for high-to-low-dose extrapolation of toxic effects of the derived mathematical relationships between administered dose and tissue dose are discussed.

Acrylamide↗
PubMedDate not supplied

Analytical methods used to measure acrylamide concentrations in foods.

The state-of-the-art of analysis for acrylamide in food is reviewed. The majority of analytical methods adopts a similar approach: addition of internal standard to the specimen, extraction with water, purification of extract using a solid-phase extraction cartridge, and then determination using either gas chromatography coupled to mass spectroscopy (GC/MS) after bromination, or direct measurement with liquid chromatography coupled to mass spectroscopy (LC/MS). The available methods generally show good agreement and are likely to be accurate. However, improvements in precision (within-laboratory) and repeatability (between-laboratory) are needed by particular data users.

Acrylamide↗