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PubMed1987

[Polymer materials for biomedical purposes obtained by radiological methods. II. Radiation polymerization of acrylamides and N-vinylpyrrolidone].

The radiation polymerization of acrylamide and N-vinylpyrrolidin-2-one in aqueous solutions has been investigated. The effect of the monomer concentration as well as the dose rate of the ionizing radiation on the process has been determined. The radical mechanism of the polymerization process has been confirmed experimentally. The effect of the individual transient species of the water radiolysis on the initiation of the polymerization process as well as the changes of the molecular weights of the arising polymers have been investigated. The dependence of the galation dose of the system on the monomer concentration has been determined.

Acrylamide↗
PubMed1986

Acrylamide produces a direct, dose-dependent and specific inhibition of oxidative metabolism in motoneurons.

The mechanism of action of acrylamide (ACR) in producing a central-peripheral distal axonopathy is unknown. We have tested the hypothesis that ACR inhibition of enzymes of oxidative metabolism is responsible for compromise of the energy supply, thereby producing the neuropathy. A single 50 mg/kg i.p. dose of ACR resulted in a 33.4% decrease in NADH-tetrazolium reductase (NADH-TR) (indicative of oxidative metabolism) activity in rat soleus motoneurons within one hour of injection. Methylene bis ACR (Mb-ACR), a non-neurotoxic analogue, produced a much smaller (6.7%) decrease in NADH-TR activity. Restoration of normal NADH-TR activity following that single injection occurred in 3 days. In vitro histochemical assays demonstrated a dose-dependent inhibition of motoneuron NADH-TR activity (10-54%) by 1-10mM ACR. Equimolar Mb-ACR produced significantly less inhibition. The rapid, dose-dependent and specific inhibition of this oxidative enzyme activity by ACR provides evidence in support of the energy hypothesis of ACR-induced neuropathy and more specifically suggests that oxidative enzyme inhibitions are a critical site of ACR action.

Acrylamide↗
PubMed1985

Direct alkylation of 2'-deoxynucleosides and DNA following in vitro reaction with acrylamide.

Reaction of the rodent carcinogen acrylamide (AM) at pH 7.0 and 37 degrees C for 10 and 40 days with 2'-deoxyadenosine (dAdo), 2'-deoxycytidine (dCyd), 2'-deoxyguanosine (dGuo), and thymidine (dThd) resulted in the formation of 2-formamidoethyl and 2-carboxyethyl adducts via Michael addition. The alkylated 2'-deoxynucleoside adducts isolated (% yield after 40 days) were 1-(2-carboxyethyl)-dAdo (1-CE-dAdo) (8%), N6-CE-dAdo (21%) (via Dimroth rearrangement of 1-CE-dAdo), 1-CE-dGuo (4%), 7-(2-formamidoethyl)-Gua (7-FAE-Gua) (6%), 7, 9-bis-FAE-Gua (1%) (formed by reaction of AM with depurinated 7-FAE-Gua during the course of the reaction), and 3-FAE-dThd (4%). The products isolated following in vitro reaction of AM with calf thymus DNA at pH 7.0 and 37 degrees C for 40 days were (nmol/mg DNA) 1-CE-dAdo (5.5), N6-CE-dAdo (1.4), 3-CE-dCyd (2.8), 1-CE-dGuo (0.3), and 7-FAe-Gua (1.6). Compound 3-FAE-dThd was not detected. Structures were assigned on the basis of chemical properties, UV spectra, and electron impact, chemical ionization, desorption chemical ionization, Californium-252 fission fragment ionization, and fast atom bombardment mass spectra. A facile hydrolysis of the amide group to a carboxylic acid was observed when AM alkylated a ring nitrogen adjacent to an exocyclic nitrogen atom. In previous studies, we had observed an analogous phenomenon when studying the in vitro reactions of acrylonitrile with DNA, i.e., a facile hydrolysis of nitrile to carboxylic acid when acrylonitrile alkylated (via Michael addition) a ring nitrogen adjacent to an exocyclic nitrogen. Since the nitrile group hydrolyzes to a carboxylic acid via an amide intermediate, we had hypothesized in the present study that the same facile hydrolysis of amide to carboxylic acid would occur under identical stereochemical conditions as had occurred with the nitrile group. Thus, in vitro alkylation of calf thymus DNA by both acrylonitrile and, in the present study, AM, resulted in mixed adduct formation.

Acrylamide↗
PubMed1985

Clinical and morphological findings in acrylamide toxicity.

Clinical features of acrylamide toxicity consist of sensorimotor peripheral neuropathy. In subacute intoxication ataxia occurs and encephalopathy also in severe acute poisoning. Slight reduction in maximal nerve conduction velocity in animals is due to degeneration of large diameter fibres. Neurofilaments accumulate within axons, both in PNS and CNS. Other changes may be important in initiation of degeneration.

Acrylamide↗
PubMed1985

Studies of the primate somatosensory system in experimental acrylamide intoxication.

Recent advances in computer-averaged electrophysiological procedures enable the noninvasive recording of activity within somatosensory fiber tracts of higher levels of the CNS in man and experimental animals. In this study, somatosensory-evoked potentials were used to trace the onset of acrylamide-induced distal axonopathy in the primate. Initial dysfunction appeared at the distal extreme of the gracile tract of the dorsal-column system. The peak latency of the SEP component at this site increased by approximately 300 us., preceded any behavioral alterations and appeared coincident with the earliest detectable morphological change in this nucleus.

Acrylamide↗
PubMed1984

Evaluation of the ability of d-penicillamine to protect rats against the neurotoxicity induced by zinc pyridinethione, acrylamide, 2,5-hexanedione and p-bromophenylacetylurea.

Dietary exposure of rats to three different concentrations of zinc pyridinethione (ZPT; 166, 332, 498 ppm) caused delayed onset failure in a treadmill test and, at the higher concentrations (332 and 498 ppm), death. Daily treatment with d-penicillamine (d-PEN) increased the latency period for treadmill failure and lethality. Comparable levels of toxicity were achieved only after d-PEN treated rats had consumed 2-3 times more ZPT than rats not treated with d-PEN. In contrast to ZPT, administration of d-PEN did not affect the onset of treadmill failure associated with acrylamide, p-bromophenylacetylurea or 2,5-hexanedione. Thus, d-PEN provided protection which was selective for ZPT.

Acrylamide↗
PubMed1983

Effect of oral CDP-choline on acrylamide-induced lesion.

Administration of low doses of cytidine diphosphate choline (CDP-choline, citicoline, Somazina) (50 mg/kg) to mice and rats has proved to be effective in preventing acrylamide-induced neurological syndrome. Likewise, the simultaneous dosing of both drugs, which causes an evident loss of weight in the animals, has demonstrated that an activation on the dopaminergic system is produced.

Acrylamide↗
PubMed1994

Acrylamide-induced distal axon degeneration: a proposed mechanism of action.

Exposure to acrylamide (ACR) monomer produces distal swelling and subsequent degeneration in central and peripheral myelinated axons of humans and laboratory animals. The molecular and cellular events leading to this type of axonopathy are currently unknown. Herein we describe a new mechanism of ACR axonopathy that represents a synthesis of recent research findings and prior hypotheses. According to this model, ion regulation in distal paranodal axon regions is compromised by diminished axolemmal Na/K-ATPase activity. It is suggested that decreased NA/K-ATPase activity is a consequence of aberrant cell body processing and/or deficient axonal transport. Reduced Na pump activity promotes membrane depolarization in conjunction with axoplasmic accumulation of Na and loss of K. Thermodynamically, this favors reverse operation of the Na/Ca-exchanger which permits axonal Ca entry in exchange for Na. The influx of Ca eventually overwhelms buffering mechanisms and leads to distal axon degeneration. Distal axons are predisposed to regulatory failure of this type due to a dependency on cell body output and the unique differential distribution of enzymes, ion channels and exchangers among nodal and internodal regions. This heuristic model might account for axon degeneration occurring as a result of exposure to other chemical neurotoxicants and following axotomy and other forms of mechanical injury.

Acrylamide↗
PubMedDate not supplied

[Biological monitoring of exposure to alkylating xenobiotics by determining them using a new analytical approach in complexes with hemoglobin, plasma proteins and mercapturic acids in urine. II. Acrylamide].

A new simple and prompt procedure for measuring acrylamide (propenamide, PA) in PA-derived mercapturic acid, such as N-acetyl-S-(2-propenamide)-L-cysteine (N-Ac-PAC), and in hemoglobin (Hb) and plasma protein adducts in the rats expose to PA was developed, by employing gas chromatography (GC). PA in mercapturic acids or proteins was liberated on high-temperature heating in an injector port during the working procedure of a GC capillary after preoxidation of sulfur atoms in PA-bound cysteine to a sulfoxide form with hydrogen peroxide and analyzed. This method resulted in 87% of PA in authentic N-Ac-PAC. The number of PA released from the protein adducts was proportional to the cumulative dose of PA given at a concentration of 1-75 mg/kg during 1-3 weeks. The alkylating level of Hb was approximately 65 times higher than that of plasma proteins and it was nearly 6.5% of its cumulative dose. The index of binding to Hb and the rate of its alkylation were 163 and 0.75.10(-3) liter/g-1/hour-1, respectively.

Acetylcysteine↗
PubMed1996

Decreased GAP-43 accumulation in neurite tips of cultured hippocampal neurons by acrylamide.

The critical axonopathy- producing effect of acrylamide (ACR) is hypothesized to be an interruption of fast vesicular transport resulting in a deficiency of distal axonal proteins. This study used the accumulation of growth associated protein- 43 (GAP-43) in neurite tips of cultured hippocampal neurons as a model to examine the effect of an ACR block of fast transport on the eventual protein concentration within the distal axon. Twenty-four hour incubation with ACR produced a dose-dependent reduction with 0.5mM and 1.0mM concentrations in the percent of neurites with a terminal GAP-43 accumulation. No change in cell size (area), cell body GAP-43 fluorescence, distal neurite fluorescence, absolute tip fluorescence or neurite length were observed. Another known inhibitor of transport, colchicine (COL) also caused a significant decrease in the percent of neurites with a GAP-43 accumulation; propionamide (PA), a non-neurotoxic analogue of ACR, had no effect on protein accumulation. These findings support the hypothesis that the disruption of fast transport by ACR can lead to depletion of vital proteins in the distal axon.

Acrylamide↗
PubMed2001

DNA sequencing by capillary electrophoresis using copolymers of acrylamide and N,N-dimethylacrylamide.

Copolymers of acrylamide (AM) and N,N-dimethylacrylamide (DMA) with AM to DMA molar ratios of 3:1, 2:1 and 1:1 and molecular weights of about 2.2 MDa were synthesized. The polymers were tested as separation media in DNA sequencing analysis by capillary electrophoresis (CE). The dynamic coating ability of polydimethylacrylamide (PDMA) and the hydrophilicity of polyacrylamide (PAM) have been successfully combined in these random copolymers. A separation efficiency of over 10 million theoretical plates per meter has been reached by using the bare capillaries without the additional polymer coating step. Under optimized separation conditions for longer read length DNA sequencing, the separation ability of the copolymers decreased with decreasing AM to DMA molar ratio from 3:1, 2:1 and 1:1. In comparison with PAM, the copolymer with a 3:1 AM:DMA ratio showed a higher separation efficiency. By using a 2.5% w/v copolymer with 3:1 AM:DMA ratio, one base resolution of 0.55 up to 699 bases and 0.30 up to 963 bases have been achieved in about 80 min at ambient temperatures.

Acrylamides↗
PubMed1992

Acrylamide monomer and peripheral neuropathy in chemical workers.

The relationship between exposure to acrylamide monomer and neurological outcomes was investigated in 82 chemical industry workers. Vibrotactile thresholds were determined quantitatively with a Vibratron II device, using forced choice and method of limits procedures. Symptoms of numbness, limb pain, peeling skin, and sweating hands had significantly higher prevalences in the exposed than in the unexposed group. Signs of peeling skin and sweating hands were significantly more common in the exposed group. Vibration thresholds were not associated with exposure.

Acrylamides↗
PubMed1979

Properties of penicillin amidase immobilized by copolymerization with acrylamide.

An enzyme preparation in a spherical granule form was obtained by copolymerization of penicillin amidase (EC 3.5.1.11) (previously modified with maleic anhydride) and acrylamide via a crosslinking agent. As compared with the native enzyme, immobilized amidase is more resistant to heating, has a lower affinity to benzylpenicillin, and is less inhibited by phenylacetate. Its substrate specificity and optimum pH remain unchanged.

Acrylamides↗
PubMed1975

[Thienyl acrylamides and thienyl pyrazolines as potential schistosomicidal agents].

Alpha-Thienyl-N-substituted acrylamides that possess analogous structures to known schistosomicidal agents were synthesized. Two chalcones were prepared by condensing alpha-thiophenealdehyde and acetophenone or its o-hydroxy derivative. Cyclization of the chalcones with hydrazine hydrate or monosubstituted hydrazines afforded 1.3.5 trisubstituted 2-pyrazoline

Acrylamides↗
PubMed2006

Effects of acrylamide, latrunculin, and nocodazole on intracellular transport and cytoskeletal organization in melanophores.

The effects of acrylamide (ACR), nocodazole, and latrunculin were studied on intracellular transport and cytoskeletal morphology in cultured Xenopus laevis melanophores, cells that are specialized for regulated and bidirectional melanosome transport. We used three different methods; light microscopy, fluorescence microscopy, and spectrophotometry. ACR affected the morphology of both microtubules and actin filaments in addition to inhibiting retrograde transport of melanosomes but leaving dispersion unaffected. Using the microtubule-inhibitor nocodazole and the actin filament-inhibitor latrunculin we found that microtubules and actin filaments are highly dependent on each other, and removing either component dramatically changed the organization of the other. Both ACR and latrunculin induced bundling of microtubules, while nocodazole promoted formation of filaments resembling stress fibers organized from the cell center to the periphery. Removal of actin filaments inhibited dispersion of melanosomes, further concentrated the central pigment mass in aggregated cells, and induced aggregation even in the absence of melatonin. Nocodazole, on the other hand, prevented aggregation and caused melanosomes to cluster and slowly disperse. Dispersion of nocodazole-treated cells was induced upon addition of alpha-melanocyte-stimulating hormone (MSH), showing that dispersion can proceed in the absence of microtubules, but the distribution pattern was altered. It is well established that ACR has neurotoxic effects, and based on the results in the present study we suggest that ACR has several cellular targets of which the minus-end microtubule motor dynein and the melatonin receptor might be involved. When combining morphological observations with qualitative and quantitative measurements of intracellular transport, melanophores provide a valuable model system for toxicological studies.

Acrylamide↗
PubMed1994

Poly(ethylene glycol)methacrylate-acrylamide copolymer media for hydrophobic protein and low temperature electrophoresis.

The properties of poly(ethylene glycol)methacrylate-acrylamide copolymer media (PEGMACs) were exploited in two ways: (i) in the first-dimensional gel of two-dimensional electrophoresis (2-DE) of hydrophobic proteins and (ii) for high speed, high-resolution electrophoresis at low temperatures. In the first application, improved resolution and yield of isoelectric focusing (IEF) separations for the hydrophobic protein zein was achieved compared to IEF in standard polyacrylamide gels. This appears promising as a candidate approach for higher resolution 2-DE mapping of uncharacterized hydrophobic proteins. In the second application, PEGMACs compatible with hydroorganic antifreeze buffer systems below cooling of the gels to low temperatures (-20 degrees C), which allowed greater current to be tolerated during electrophoresis. PEGMAC gels enabled us to perform sixfold faster electrophoretic separations and achieve threefold improved resolution of six standard proteins at the lower temperatures in a direct comparison with the normal sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) system. If this approach is coupled with more precise instrumentation to control low temperatures during electrophoresis, greater separation speeds and resolution may be anticipated.

Acrylamides↗
PubMed1997

Capillary electrophoretic separation of structurally similar solutes in noncross-linked poly(acrylamide-co-N-isopropylacrylamide) solution.

Noncross-linked acrylamide (AA)-N-isopropylacrylamide (IPAAm) copolymers have been used as a buffer additive in capillary electrophoretic separation of structurally similar small solutes. Seven kinds of barbiturates and five kinds of dansylated (Dns) amino acids, which have different hydrophobic side chains, were separated on poly(AA-co-IPAAm)-filled columns and on AA polymer-filled columns under the condition of totally eliminating the contribution of electroosmotic flow (EOF). It is known that the copolymer containing IPAAm has thermosensitive properties, and the hydrophobicity of its surface changes with surrounding temperature. In this investigation, therefore, the effects of an isopropyl group in the copolymer on the electrophoretic separation of the small solutes were studied by comparing the two polymer-filled columns at ambient temperature and at elevated temperature. Although slight differences in migration behavior were observed at ambient temperature between the columns filled with these two polymer solutions, obvious differences in the separation of the solutes were observed at elevated temperature. The observed changes on the migration behavior might be caused by the interaction between copolymer chains exhibiting hydrophobic property and the solute.

Acrylamides↗
PubMed2006

Genotoxicity of acrylamide and its metabolite glycidamide administered in drinking water to male and female Big Blue mice.

The recent discovery of acrylamide (AA), a probable human carcinogen, in a variety of fried and baked starchy foods has drawn attention to its genotoxicity and carcinogenicity. Evidence suggests that glycidamide (GA), the epoxide metabolite of AA, is responsible for the genotoxic effects of AA. To investigate the in vivo genotoxicity of AA, groups of male and female Big Blue (BB) mice were administered 0, 100, or 500 mg/l of AA or equimolar doses of GA, in drinking water, for 3-4 weeks. Micronucleated reticulocytes (MN-RETs) were assessed in peripheral blood within 24 hr of the last treatment, and lymphocyte Hprt and liver cII mutagenesis assays were conducted 21 days following the last treatment. Further, the types of cII mutations induced by AA and GA in the liver were determined by sequence analysis. The frequency of MN-RETs was increased 1.7-3.3-fold in males treated with the high doses of AA and GA (P < or = 0.05; control frequency = 0.28%). Both doses of AA and GA produced increased lymphocyte Hprt mutant frequencies (MFs), with the high doses producing responses 16-25-fold higher than that of the respective control (P < or = 0.01; control MFs = 1.5 +/- 0.3 x 10(-6) and 2.2 +/- 0.5 x 10(-6) in females and males, respectively). Also, the high doses of AA and GA produced significant 2-2.5-fold increases in liver cII MFs (P < or = 0.05; control MFs = 26.5 +/- 3.1 x 10(-6) and 28.4 +/- 4.5 x 10(-6)). Molecular analysis of the mutants indicated that AA and GA produced similar mutation spectra and that these spectra were significantly different from that of control mutants (P < or = 0.001). The predominant types of mutations in the liver cII gene from AA- and GA-treated mice were G:C-->T:A transversions and -1/+1 frameshifts in a homopolymeric run of Gs. The results indicate that both AA and GA are genotoxic in mice. The MFs and types of mutations induced by AA and GA in the liver are consistent with AA exerting its genotoxicity in BB mice via metabolism to GA.

Acrylamide↗