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PubMed1992

Acrylamide disrupts elemental composition and water content of rat tibial nerve. II. Schwann cells and myelin.

The effects of subchronic and subacute acrylamide (ACR) intoxication on elemental composition (Na, P, S, Cl, K, Ca, Mg) and water content of Schwann cell body cytoplasm and myelin were assessed in rat tibial nerve. Electron probe X-ray microanalysis demonstrated that, in control rats, peripheral nerve glia and myelin exhibited highly characteristic distributions of elements and water and that ACR intoxication was associated with disruption of this normal subcellular distribution. When rats were intoxicated with ACR by either the oral (2.8 mM in drinking water for 15, 22, 30, and 60 days) or the intraperitoneal (50 mg/kg/day x5 and 10 days) route, an exposure-dependent loss of cytoplasmic Na, K, P, Cl, Mg, and water regulation was detected in Schwann cell cytoplasm. Maximum development of elemental deregulation occurred after 30 days of oral ACR exposure and 10 days of ip treatment. The cytoplasmic elements involved and their corresponding quantitative changes were similar regardless of the route of ACR intoxication. Analysis of myelin revealed that both oral and parenteral ACR exposure caused early, persistent increases in dry weight Na, P, and water content. However, Cl dry weight concentrations were increased by oral exposure and decreased by ip ACR injection. Results of this study indicate that ACR intoxication is associated with a significant disturbance of subcellular element and water distribution in tibial nerve Schwann cells and myelin. The pattern of elemental disruption is typical of reversible cell damage and, therefore, Schwann cell injury might play a role in the expression of ACR neurotoxicity.

Acrylamide↗
PubMed1996

In vitro swelling studies and preliminary biocompatibility evaluation of acrylamide-based hydrogels.

In this in vitro study, the biocompatibility of acrylamide-based hydrogels such as acrylamide/crotonic and acrylamide/itaconic acid, prepared by using gamma-rays, has been investigated against some biochemical parameters of human serum. The swelling kinetics of acrylamide/crotonic and acrylamide/itaconic acid hydrogels are investigated in distilled water and physiological saline solution and some swelling and diffusion parameters have been calculated. For the analysis of biocompatibility, acrylamide/crotonic and acrylamide/itaconic acid hydrogels are incubated in 10 different human sera for 24 h and their biocompatibilities with some biochemical parameters have been investigated. No significant difference in values before and after the test procedures have been found. It is therefore concluded that acrylamide/crotonic and acrylamide/itaconic acid hydrogels are biocompatible.

Acrylamide↗
PubMed1984

Circulatory control in canine acrylamide neuropathy.

The baroreflex regulation of arterial blood pressure and heart rate was examined in dogs with acrylamide-induced peripheral neuropathy. In anaesthetized animals the carotid sinuses were isolated from the systemic circulation and perfused. The carotid sinus and vagus nerves were kept intact. The maximum baroreflex gain (the ratio of the change in systemic pressure to a change in sinus pressure) was significantly greater in the treated animals. A step increase in carotid sinus pressure produced long periods of asystole and sustained bradycardia in the animals with neuropathy. The alterations in the baroreceptor reflex responses were consistent with dysfunction of baroreceptor fibres in the vagus.

Acrylamide↗
PubMed1991

Induction of specific-locus mutations in male germ cells of the mouse by acrylamide monomer.

Acrylamide monomer (AA), injected into male mice at the maximum tolerated dose of 5 x 50 mg/kg (24-h intervals), significantly increased the specific-locus mutation rate in certain poststem-cell stages of spermatogenesis, but not in spermatogonial stem cells. Germ-cell stages in which the treatment induced dominant lethals--namely, exposed spermatozoa and late spermatids (number of surviving offspring only 3% and 27%, respectively, of those in concurrent controls)--jointly yielded the highest frequency of specific-locus mutations. AA thus conforms to Pattern 1 in our earlier classification of chemicals according to the spermatogenic stage at which they elicit maximum response (Russell et al., 1990). No specific-locus mutations were observed among 17,112 offspring derived from exposed spermatogonial stem cells, a result which rules out (at the 5% significance level) an induced mutation rate greater than 2.3 times the historical control rate. A sustained high productivity in matings made for several months following week 3 indicates that there is no significant spermatogonial killing and that cell selection is presumably not the explanation for the negative result. On the basis of genetic and/or cytogenetic evidence, the mutations induced postmeiotically by AA were 'large lesions' (multi-locus), while one of 2 recovered from exposure of differentiating spermatogonia is probably a small lesion. An earlier survey of mammalian mutagenesis results led us to conclude that, regardless of the classification of a chemical according to the stage at which it elicits its maximum response, the nature of mutations is determined by the germ-cell stage in which they are induced (Russell et al., 1990). The AA results on lesion size and on distribution of mutations among the loci fit the general pattern.

Acrylamide↗
PubMed1993

Perturbation of cell division by acrylamide in vitro and in vivo.

Exposure of V79 Chinese hamster cells to acrylamide (AA) caused a concentration-dependent increase in the incidence of spindle disturbances. A c-mitotic effect with the appearance of C-metaphases, a mitotic block and the concomitant disappearance of ana-telophase figures, was observed after 6 h of treatment with concentrations ranging from 0.01 to 1.0 mg/ml of AA. Intraperitoneal injection of male mice with the highest tolerated dose of 120 mg/kg of AA showed no mitotic arrest in bone marrow cells. However, 1 h and 3 h after treatment the frequencies of cells with highly condensed and separated chromatids was reduced indicating an effect on mitotic progression. In spermatocytes of mice AA caused a meiotic delay from 2 h to 22 h after treatment determined by a reduced ratio of second/first meiotic divisions. The meiotic delay was predominantly due to a prolongation of interkinesis. The present results show that AA causes disturbances of cell division in vitro and in vivo. They suggest that AA might induce aneuploidy in mammalian cells in vitro by interfering with proper functioning of the spindle similar to the effect of colchicine. In vivo, particularly in spermatocytes, the progression of cell division was altered by AA. It cannot be explained simply by an effect on spindle function, however, this alteration may also cause errors in chromosome segregation.

Acrylamide↗
PubMed1990

Developmental toxicity evaluation of acrylamide in rats and mice.

Acrylamide (ACRL), a widely used industrial chemical with neurotoxic effects, was evaluated for developmental toxicity. ACRL in distilled water was administered once daily by gavage on gestational days (gd) 6-17 to mice (0, 3, 15, or 45 mg/kg) and on gd 6-20 to rats (0, 2.5, 7.5, or 15 mg/kg). Following termination (gd 17, mice; gd 20, rats) fetuses were examined for external, visceral, and skeletal malformations. Maternal toxicity during treatment was observed at the highest dose as reduced body weight gain in both species and hindlimb splaying in treated mice only. Weight gain corrected for gravid uterine weight was also reduced in rats at 7.5 and 15 mg/kg/day. Embryo/fetal toxicity was not observed in rats, but fetal weight was reduced in mice administered 45 mg/kg/day. No increase in the incidence of malformations was observed in either species; however, the incidence of variations (predominately extra rib) increased with dose. In summary, administration of ACRL during organogenesis produced maternal and developmental toxicity at 45 mg/kg/day in mice and maternal, but not developmental, toxicity at doses greater than or equal to 7.5 mg/kg/day in rats.

Acrylamide↗
PubMed1991

A neurotoxicity screening battery for use in safety evaluation: effects of acrylamide and 3',3'-iminodipropionitrile.

The effects of two known neurotoxicants, acrylamide (ACR) and 3',3'-iminodipropionitrile (IDPN), were assessed using a functional observational battery (FOB), a measurement of motor activity (MA), and neuropathology (NP) in the context of a safety evaluation study. One hundred Sprague-Dawley rats (10/sex/group) were tested initially and then doses with vehicle, ACR (10 or 30 mg/kg/day), or IDPN (50 or 125 mg/kg/day) by oral gavage 7 days/week for 5 weeks (except where otherwise indicated). Neurobehavioral assessments were conducted prior to initiating treatment at 1, 6, and 24 hr after the first dose, and weekly thereafter. Body weight and food consumption were determined weekly, and animals were observed twice daily for signs of toxicity. Blood samples were obtained at termination for routine clinical pathology studies. At termination three animals/sex/group were perfused in situ for neuropathology evaluations and the remaining animals were necropsied for standard histological evaluations. Prominent neurological signs were observed in high-dose animals after 2 weeks, and significant mortality occurred in high-dose ACR animals during Week 3. A 7- or 10-day recovery period was initiated after 20 or 22 daily doses for high-dose IDPN and ACR animals, respectively. ACR and IDPN affected body weight, body-weight gain, food consumption, general activity (horizontal and vertical), urination, muscle tone (grip strength), motor reflexes, gait, and posture. Significant sex effects were seen in animals exposed to IDPN, with males being more severely affected. Microscopic examination of nervous system tissue and selected organs revealed minimal to moderately severe axonal swelling characterized by the presence of enlarged balloon-like axons in the brainstem and the cervical and lumbar cord of IDPN-treated animals. This change was most prominent in males and most severe in the lumbar spinal cord. An increased incidence of chronic progressive nephropathy was also noted in IDPN-treated rats. ACR-treated animals exhibited minimal to moderate degeneration in the cervical and lumbar spinal cord, the gasserian and dorsal root ganglia, and the tibial, sciatic, and sural nerves which were characterized by changes in axonal diameter, increased argyrophilia of axons, and disruption, fragmentation, and distortion of axons and the myelin sheath. Granulomatous inflammation in the lungs of high-dose ACR animals resulted from inhalation of feed, most probably due to partial paralysis or incoordination during feeding.

Acrylamide↗
PubMed1992

Comparison of subchronic neurotoxicity of 2-hydroxyethyl acrylate and acrylamide in rats.

The comparative neurotoxicity of subchronic exposure to 2-hydroxyethyl acrylate (HEA) and acrylamide (ACR) was evaluated using a functional observational battery (FOB) and neuropathology. Three dose levels of each compound (HEA: 3, 20, 60 mg/kg; ACR: 1, 4, 12 mg/kg) were administered intraperitoneally to male and female Long-Evans rats (n = 10/sex/dose level), 5 days/week for 13 weeks. Two vehicle control groups were also included. The FOB, which includes home-cage and open-field observations and interactive tests of sensory, neuromuscular, and autonomic function, was administered before dosing, at monthly intervals, and on the day after the last dose. Subsets of rats (n = 6/sex/dose level) were then perfused and tissues from the brain, spinal cord, and peripheral nerve were prepared for light microscopic evaluation. There were clear differences between the effects of HEA and ACR. ACR produced time- and dose-related changes in FOB measures of muscle tone and equilibrium, and produced axonal degeneration in peripheral nerves and within long tracts of the spinal cord. HEA exposure was also associated with changes in muscular function on FOB testing, but the magnitude of the effects was not as great as with ACR and not dose related. In addition, no neuropathological changes were detected after HEA exposure. Thus, the effects of HEA did not resemble those of ACR. The FOB data were summarized in domains of neurobehavioral functions. Using a composite score analysis, ACR was shown to produce prominent effects in the neuromuscular domain whereas HEA was largely without effect. When the data are analyzed in this manner, the neurotoxic potential of HEA appears to be minimal.

Acrylamide↗
PubMed1986

In vitro transformation of C3H/10T1/2 and NIH/3T3 cells by acrylonitrile and acrylamide.

Acrylonitrile (AN) and acrylamide (AM) are carcinogenic in a number of rodent organs and AN is a suspected human carcinogen. We sought to determine whether AN and/or AM could produce morphological transformation in vitro in C3H/10T1/2 and NIH/3T3 mouse fibroblast cells. Both AN and AM induced a dose-dependent cytotoxic effect in C3H/10T1/2 and NIH/3T3 cells and readily transformed both cell lines. Our conclusions are based on the appearance of cells exhibiting a transformed phenotype and growth in soft agar. AN and AM transformed NIH/3T3 cells to a greater extent than C3H/10T1/2 cells. This is the first reported transformation of cells in vitro by AM.

Acrylamide↗
PubMed1986

Paradoxical changes in spinal cord reflexes following the acute administration of acrylamide.

Acrylamide (ACR) produces a central-peripheral distal axonopathy when administered chronically. This is characterized functionally by decreases in the monosynaptic reflex (MSR) and dorsal root potential (DRP) and alterations in the characteristics of the dorsal root reflex (DRR). Acute administration of ACR inhibits the oxidative enzyme complex NADH-tetrazolium reductase and slows retrograde axoplasmic transport. This study was carried out to determine if the spinal cord reflexes are also affected following acute administration of ACR. Dose-response studies revealed a dose-dependent increase in both the MSR and DRR. A single injection of 50 mg/kg ACR caused an increase in both the MSR and DRR within 15 min and continued for over 3 h. These data are paradoxical since chronic administration of ACR results in decreased function. Two possible mechanisms are proposed. First, calcium ion regulation may be involved in both the acute and chronic effects of ACR on spinal cord reflexes. Second, a depolarization of the neurons is occurring just prior to cell injury or death.

Acrylamide↗
PubMed1996

Release of 5-fluorouracil from poly(acrylamide-co-monopropyl itaconate) hydrogels.

The aim of this work was to test the application of copolymeric poly(acrylamide-co-monopropyl itaconate) (A-MPI) hydrogels on the release of 5-fluorouracil (5-FU). The equilibrium degree of swelling in saline solution was 83 +/- 2%. 5-FU, as the sodium salt, was trapped in gels by placing it in the polymerization feed mixture. The diffusion coefficients for both swelling of the gels and the release of 5-FU were determined, in addition to the activation energies for both processes. To determine the applicability of these copolymers, A-MPI (75:25) gel was subcutaneously implanted in rats and the drug plasma concentration was determined by HPLC.

Acrylamide↗
PubMed1986

Interaction of acrylamide with bovine serum albumin.

The binding of acrylamide (ACR) with purified bovine serum albumin (BSA) was studied. Binding of ACR with BSA was characterized by equilibrium dialysis, fluorescence studies, and ultraviolet spectroscopy. ACR was quantitated by high-pressure liquid chromatography. Equilibrium dialysis studies on the binding of ACR with BSA showed that more than 25% of the added ligand was bound to the protein at equilibrium. ACR produced a concentration-dependent decrease in uv absorbance of BSA, indicating reactivity of ACR with BSA. Fluorescence quenching studies of ACR binding showed a concentration-dependent quenching of the fluorescence of BSA. ACR also caused a concentration-dependent decrease in the fluorescence of sulfhydryl (-SH) groups present on BSA, implicating a role of protein -SH groups in the binding of ACR. Prior blocking of -SH groups by N-ethylmaleimide resulted in 16% inhibition of the initial binding of ACR, suggesting involvement of -SH groups. Our results demonstrate that ACR binds to BSA through both aromatic amino acids and -SH groups and that such binding may play an important role in pharmacodynamics and toxicity of ACR.

Acrylamide↗
PubMed2002

Hemoglobin adducts and micronucleus frequencies in mouse and rat after acrylamide or N-methylolacrylamide treatment.

The reactive industrial chemicals acrylamide (AA) and N-methylolacrylamide (MAA) are neurotoxic and carcinogenic in animals, MAA showing a lower potency than AA. The causative agent in AA-induced carcinogenesis is assumed to be the epoxy metabolite, glycidamide (GA), which in contrast to AA gives rise to stable adducts to DNA. The causative agent in MAA induced carcinogenesis is so far not studied. The two AAs were studied in mice and rats using analysis of hemoglobin (Hb) adducts as a measure of in vivo doses and the in vivo micronucleus (MN) assay as an end-point for chromosome damage. Male CBA mice were treated by intraperitoneal (i.p.) injection of three different doses and male Sprague-Dawley rats with one dose of each AA. Identical adducts were monitored from the two AAs [N-(2-carbamoylethyl)valine] and the respective epoxide metabolites [N-(2-carbamoyl-2-hydroxyethyl)valine]. Per unit of administered amount, AA gives rise to higher (three to six times) Hb adduct levels than MAA in mice and rats. Mice exhibit, compared with rats, higher in vivo doses of the epoxy metabolites, indicating that AAs were more efficiently metabolized in the mice. In mouse the two AAs induced dose-dependent increases in both Hb adduct level and MN frequency in peripheral erythrocytes. Per unit of administered dose MAA showed only half the potency for inducing micronuclei compared with AA, although the MN frequency per unit of in vivo dose of measured epoxy metabolite was three times higher for MAA than for AA. No increase in MN frequency was observed in rat bone marrow erythrocytes, after treatment with either AA. This is compatible with a lower sensitivity of the rat than of the mouse to the carcinogenic action of these compounds.

Acrylamide↗
PubMed1992

Acrylamide polymerization kinetics in gel electrophoresis capillaries. A Raman microprobe study.

The formation of 3.5% T, 3.3% C cross-linked polyacrylamide is monitored in 75-microns-i.d. electrophoresis capillaries by Raman microprobe spectroscopy. The disappearance of the acrylamide 1292-cm-1 band is followed with 60-s time resolution for 30 min, and 2-4 min resolution for up to 10 h. Polymerization is 98% complete in 1.5 h and greater than 99% complete after 2 h. In the 900-1700-cm-1 region no bands attributable to cross-linking are observable. Reaction in the capillary follows second-order kinetics. The reaction is faster in the bulk system because heat dissipation is not sufficient to maintain a constant temperature.

Acrylamide↗
PubMed1988

Quenching of tryptophanyl fluorescence of bovine adrenal P-450C-21 and inhibition of substrate binding by acrylamide.

Quenching of the tryptophanyl fluorescence of cytochrome P-450C-21 by acrylamide and its relationship to substrate binding are investigated by using steady-state and time-resolved data. The average collisional quenching constant was 0.4 M whereas the quenching constant for the total fluorescence was 10.8 +/- 0.9 M. This indicates that the quenching is essentially static. The quencher inhibited the binding of the substrate apparently competitively. The inhibition constant was 0.092 M, giving rise to an association constant of 10.9 M which is remarkably similar to the static quenching constant. It is suggested that tryptophan(s) may represent a key to the substrate-binding site in P-450C-21.

Acrylamide↗
PubMed1997

Urinary metabolites from F344 rats and B6C3F1 mice coadministered acrylamide and acrylonitrile for 1 or 5 days.

The purpose of this study was to examine the feasibility of using 13C NMR spectroscopy to analyze urinary metabolites produced following coadministration of two structurally similar carbon-13-labeled compounds to rodents. Acrylonitrile (AN) and acrylamide (AM) are used in the chemical industry to manufacture plastics and polymers. These compounds are known to produce carcinogenic, reproductive, or neurotoxic effects in laboratory animals. The potential for human exposure to AN and AM occurs in manufacturing facilities and environmentally. Male F344 rats and B6C3F1 mice were coadministered po [1,2,3-13C]AN (16-17 mg/kg) and [1,2,3-13C]AM (21-22 mg/kg) after 0 or 4 days of administration of unlabeled AN or AM. Urine was collected for 24 h following administration of the 13C-labeled compounds and analyzed by 13C NMR spectroscopy. Rats and mice excreted metabolites derived from glutathione (GSH) conjugation with AM or AN or derived from GSH conjugation with the epoxides cyanoethylene oxide (CEO) or glycidamide (GA). GA and its hydrolysis product were also detected in the urine of rats and mice. For mice, an increased urinary excretion of total AN- and total AM-derived metabolites (p < 0.05) on repeated coadministration suggested a possible increase in metabolism via oxidation. In addition, mice had an increased (p < 0.05) percentage of dose excreted as metabolites derived from GSH conjugation with AM, AN, CEO, or GA after five exposures as compared with one exposure that may be related to a significant increase in the synthesis of GSH or an increase in glutathione transferase activity. The only significant (p < 0.05) increase between one and five exposures for the rat was in the percentage of metabolites produced following conversion of AM to GA. The use of 13C NMR spectroscopy has provided a powerful methodology for elucidation of the metabolism of two 13C-labeled chemicals administered simultaneously.

Acrylamide↗
PubMed2000

Acrylamide: a cooking carcinogen?

Exposure to acrylamide (AA) has been monitored by mass spectrometric detection of the adduct, N-(2-carbamoylethyl)valine (CEV), to the N-termini of hemoglobin (Hb), according to the N-alkyl Edman method. In these studies, a conspicuous background level, about 40 pmol/g of globin, of apparently the same adduct was regularly observed in Hb from persons without known exposure to AA. For testing of the hypothesis that this adduct originates from AA formed in cooking, rats were fed fried animal standard diet for 1 or 2 months. These animals exhibited a strong increase of the level of the studied Hb adduct, compared to control rats fed unfried diet. By gas chromatography/tandem mass spectrometry, the identity with CEV was confirmed by the concordance of the product ion spectrum of the studied adduct with that of a verified standard and by interpretation of the fragment ions. Further support of the chemical structure, at the same time pinpointing AA as the causative reactive factor, was obtained through the demonstration that AA is formed in the heating of the feed and that the level of AA in the fried feed is compatible with the measured levels of the CEV adduct. The raised CEV adduct levels observed in experimental animals are of a magnitude that is similar to the background level in nonsmoking humans. These data render it likely that cooking of food is a major source of the background dose of AA also in humans. An evaluation of cancer tests of AA and available data for its metabolism leads to the estimation that the background dose of AA is associated with a considerable cancer risk.

Acrylamide↗
PubMed1986

Reproductive toxicity associated with acrylamide treatment in male and female rats.

The present study was designed to evaluate the influence of acrylamide (ACR) on male and female reproductive function. Male rats received ACR in drinking water (50, 100, or 200 ppm) for up to 10 wk. Copulatory behavior, semen, and (for controls and 100 ppm only) fertility and fetal outcomes were evaluated. Females received ACR (25, 50, 100 ppm) for 2 wk prior to initiation of breeding and then throughout gestation and lactation. Hindlimb splaying was apparent in the 200-ppm males by wk 4; less severe splaying appeared in the 100-ppm group at wk 8. Disruptions in copulatory behavior preceded the appearance of this ataxia. These disruptions in mating performance interfered with ejaculatory processes and subsequent transport of sperm, since semen was found in the uterus of only 1 of the 15 females mated with the 100-ppm males at wk 9. Moreover, only 33% of the females mated (wk 10) to the 100-ppm males were pregnant. Postimplantation loss was also significantly increased in this group. Hindlimb splaying appeared in the females receiving 100 ppm ACR during wk 1-2 of pregnancy. Body weight and fluid intake were also depressed. Dams in the 50-ppm group showed depression in these parameters during the last 2 wk of lactation. ACR did not significantly affect mating performance of the females, pregnancy rates, litter size, or survival. However, ACR did significantly depress pup body weight at birth (100-ppm group) and weight gain during lactation through post-weaning, d 42 (50- and 100-ppm groups). Vaginal patency was delayed in the 100-ppm group only.

Acrylamide↗