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PubMed1989

Acrylamide binding to the DNA and protamine of spermiogenic stages in the mouse and its relationship to genetic damage.

Mice received an intraperitoneal injection of 14C-labeled acrylamide (AA) at an exposure of 125 mg/kg to equal that used in genetic studies carried out by Shelby et al. (1986). Subsequently, spermatozoa were recovered from the reproductive tracts of the animals over a 3-week period and assayed for the amount of bound AA. A strong increase in the level of binding occurred in late-spermatid to early-spermatozoa stages; these same stages are also genetically most sensitive to the action of AA. At all time points, alkylation of DNA within the sperm accounted for a very small fraction (generally less than 0.5%) of the total sperm-head alkylation. However, alkylation of protamine, a protein unique to sperm cells, was found to be correlated with total sperm-head alkylation and accounted for essentially all of the AA binding. Two radioactive adducts were found in hydrolysed protamine samples, one of which co-eluted with a standard of S-carboxyethylcysteine. Protamine alkylation appears to be a significant cause of acrylamide-induced genetic damage in spermiogenic cells of the mouse.

Acrylamide↗

PubMed1986

Dominant lethal effects of subchronic acrylamide administration in the male Long-Evans rat.

Acrylamide, a widely used vinyl monomer, is well known as a neurotoxin but inactive as a mutagen in bacterial test systems. The experiments reported demonstrate that after subchronic oral dosing in the male rat, acrylamide induced significant elevations in both pre- and post-implantation loss following dominant lethal testing. These effects were seen at doses which failed to produce clinical or pathological evidence of neurotoxicity. In an accompanying cytogenetic study, no increase in chromosome aberrations was observed in spermatogonia or spermatocytes of treated animals. When spermatocytes from treated spermatogonial stem cells were analyzed, reciprocal translocations (4) were observed in the treated animals and not in the control, but the significance of this result still needs to be established.

Acrylamide↗

PubMedDate not supplied

Cytogenetic effects of acrylamide in the bone marrow of mice.

A single i.p. injection of 100 mg/kg acrylamide monomer elevated the frequency of chromosome aberrations and micronucleated polychromatic erythrocytes in the bone marrow of male ICR mice. A positive relationship between frequency of micronuclei and dose of acrylamide was obtained in the dose range of 2 x 25, 2 x 50 and 2 x 100 mg/kg.

Acrylamide↗

PubMed1992

Kinetochore-staining of spermatid micronuclei: studies of mice treated with X-radiation or acrylamide.

The rodent spermatid micronucleus (MN) assay was used in conjunction with immunofluorescent techniques to distinguish kinetochores in MN following exposure of mice to X-radiation or acrylamide. After either treatment, modest increases in kinetochore-positive MN were observed. Spermatids which had been exposed during meiotic prophase to X-rays (400 cGy) had approximately 10-fold increases in MN compared to controls; up to 15% of the MN observed were kinetochore-positive. Following acrylamide treatment of meiotic prophase cells, there was a doubling of spermatid MN over baseline levels, approximately one-third of which were kinetochore-positive.

Acrylamide↗

PubMed1992

Enzymatic synthesis of acrylamide: a success story not yet over.

The application of enzymatic transformations is attracting increasing attention. Until recently, such an approach has generally been confined to producing fine chemicals difficult to obtain through conventional chemical methods. Microbial nitrile hydratase (NHase) has now been applied to the industrial, kiloton-scale production of the important chemical commodity acrylamide. Recent progress in understanding microbial nitrile metabolism at both the gene and protein levels is permitting improvement of the acrylamide production process.

Acrylamide↗

PubMed1988

Low protein diet modifies acrylamide neurotoxicity.

The present study deals with the role of protein deficiency in the neurobehavioural effects of acrylamide in rat pups exposed during pregnancy and early infancy. The data indicated that acrylamide could be more toxic in protein-deficient hosts as it significantly decreased the dopamine and benzodiazepine receptor binding and delayed the development of reflexes and land marks in these pups.

Acrylamide↗

PubMed1988

Immunochemical studies of acrylamide-associated neuropathology.

An immunohistochemical study on neurofilaments (NF) in the central and peripheral nervous systems of rats after repeated treatment with acrylamide was done by the avidin-biotin complex method using monoclonal anti-neurofilaments antibodies (68, 160 and 200 kD). Rats were given acrylamide (50 ml/kg) i.p. every day for 8 days. In the cerebrum, NF in perikarya of large nerve cells were weakly stained with all antibodies in both control and treated rats, with no differences between the 2 groups. In the cerebellum, NF of the Purkinje cells were slightly stained with all 3 antibodies. In the treated rats, a marked accumulation of NF in the distal part of the basket cell fibers was detected by 68 kD. In the molecular layer, some parallel fibers were also stained by 68 kD in the treated animals. In the spinal cord, all NF were stained, the staining being clearer in the lower part of the cord in the treated rats. In the peripheral nerve of the treated rats, many axons were segmentally swollen along the entire length of the nerve, especially, in the distal region. In muscle preparations of the treated rats, some neuro-muscular junctions stained with 68 kD were also visible.

Acrylamide↗

PubMed1993

Subcellular distribution and immunological detection of retrograde axonally transported proteins in acrylamide and diabetic neuropathies.

Neuropathies produced by both acrylamide- and streptozotocin-induced diabetes in the rat are accompanied by a deficit in the retrograde axonal transport of a defined group of proteins that can be visualized on two-dimensional polyacrylamide gels. In this work, these proteins are identified as being primarily soluble and being absent from rat brain. They are not immunologically related to the major retrogradely transported protein synaptophysin. Polyclonal antiserum to the proteins was produced in mice and used to confirm the reduction in their retrograde transport in sciatic nerve of diabetic and acrylamide-treated rats.

Acrylamide↗

PubMed1983

Acrylamide-induced changes in the monoamines and their acid metabolites in different regions of the rat brain.

Acrylamide administration of 10 and 20 mg/kg body weight i.p. in the male rat induced alteration in the levels of dopamine (DA), serotonin (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) in different regions of the brain. Selective but widespread changes were observed in 5-HIAA levels in all regions of the brain studied. 5-HT levels were significantly increased in the brain stem. The DA content also showed a significant increment in the caudate nucleus. These data suggested that the neurotoxicity of acrylamide might be correlated with the overall disturbances of serotonergic system.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1984

Acid hydrolases in brain, spinal cord and sciatic nerves of acrylamide-intoxicated rats.

Activity of beta-glucuronidase and cathepsin-D were studied in brain, spinal cord and sciatic nerves of rats at 24 h or 10 days after daily i.p. administration of 50 mg/kg acrylamide. The activities of beta-glucuronidase and cathepsin-D in brain, spinal cord and sciatic nerves remained unaffected on single exposure but increased significantly in these tissues on administration of the neurotoxin for 9 consecutive days. The increase in the activity of beta-glucuronidase and cathepsin-D was more marked in sciatic nerves, than brain or spinal cord. These results suggest that cathepsin-D and beta-glucuronidase may be involved in the acrylamide-induced degeneration of nervous tissues and can serve as useful markers for the detection of chemical-induced neuropathies.

Acrylamide↗

PubMed1984

Cytotoxicity of cyclophosphamide and acrylamide in glioma and neuroblastoma cell lines cocultured with liver cells.

A method for the cocultivation of nervous system cells with liver cells has been developed. When acrylamide was tested using the cocultivation procedure no significant liver metabolism-mediated changes in the cytotoxicity in C6 culture were detected. In neuroblastoma N1E115 cultures the toxicity was increased by induced chick hepatocytes at high acrylamide concentrations.

Acrylamide↗

PubMed1992

Toxic neurofilamentous axonopathies and fast anterograde axonal transport. IV. In vitro analysis of transport following acrylamide and 2,5-hexanedione.

Recent investigations into the mechanisms of neurotoxicity of acrylamide and gamma-diketones have demonstrated reductions in the delivery of radiolabelled proteins to the distal axon. To differentiate a toxicant-induced compromise in the capacity of the fast anterograde axonal transport system from a neuron cell body processing effect, selective exposure of either the L5 dorsal root ganglion or sciatic nerve to 0.7 mM acrylamide (ACR) or 4 mM 2,5-hexanedione (2,5-HD) was performed during in vitro transport. Nerve exposure to ACR decreased the quantity of transport by 32%, 2,5-HD reduced the quantity by 44%. Ganglion exposure produced no significant changes. We conclude that both toxicants penetrate the nerve barriers and act directly and/or indirectly on the axonal transport mechanisms to cause the reductions in transport.

Acrylamide↗

PubMedDate not supplied

Developmental neurotoxicity evaluation of acrylamide in Sprague-Dawley rats.

Based on the literature to-date, the potential of acrylamide (ACRL) to cause developmental neurotoxicity in laboratory animals has not been assessed. We examined this potential in Sprague-Dawley rats using a study design similar to that proposed by the USEPA. Dosages of 0 (deionized water), 5, 10, 15, or 20 mg/kg/day were administered at 5 ml/kg by oral gavage from gestational day 6 to lactational day 10 to groups of 12 mated females each. Females were allowed to deliver and the offspring were evaluated for survival, growth, development, behavior, and histological changes to brain, spinal cord, and peripheral nerve. Behavioral assessments consisted of open-field motor activity, auditory startle habituation, and passive avoidance tests during both the preweaning and adult periods (1 animal/sex/litter). All F0 and F1 animals in the 20 mg/kg/day group were euthanized early in the lactation period due to high pup mortality. Significantly increased pup mortality was also present in the 15 mg/kg/day group. There were dose-related decreases in average F0 maternal body weight gains during the dosing period in the 10, 15, and 20 mg/kg/day groups, and characteristic hindlimb splaying was observed in dams of the two highest dosage groups. Pup body weight proved to be the most sensitive indicator of developmental toxicity. Dose-related decrease in preweaning average weights were observed at all dose levels, although only transiently in the 5 mg/kg/day group. Average weight gain during the postweaning period was significantly decreased only in males of the 15 mg/kg/day group. Significant decreases in average horizontal motor activity and auditory startle response were observed only in weanlings of the 15 mg/kg/day group. The only behavioral effect in F1 adult animals was a decrease in auditory startle response in females of the 15 mg/kg/day group. There were no effects in the passive avoidance test or in the histological examination of the nervous system of preweaning pup or adult animals. Based on these results, the NOAEL (No Observed Adverse Effect Level) for developmental toxicity is less than 5 mg/kg/day, the NOAEL for maternal toxicity is 5 mg/kg/day, and that for developmental neurotoxicity is 10 mg/kg/day. Thus behavioral changes in the offspring were observed only at a dose which was also maternally toxic. These results suggest that acrylamide may be a selective developmental toxicant but not a selective developmental neurotoxicant, because a conventional measure of offspring toxicity (i.e., pup body weight) was affected at a dosage lower than that which produced maternal effects or offspring behavioral effects.

Acrylamide↗

PubMed1997

Early growth of regenerating neurites in acrylamide neuropathic mice: application of a film model.

Acrylamide intoxication markedly impairs neural regeneration following transection of a peripheral nerve. However, no neural inhibitory mechanism has yet been clarified. In the present study, the early growth of regeneration neurites in acrylamide neuropathic mice was analyzed using a film model: following transection of the common peroneal nerve, the proximal stump was sandwiched between two sheets of thin plastic film and kept in vivo for various intervals after axotomy. The regenerating axons grew for a significantly (P < 0.01) longer distance than those in the controls up to the 2nd day after axotomy (day 2), but thereafter the axons showed suppressed growth. Many disoriented neurofilaments were already accumulated in the axons on day 1, and their number progressively increased. The number of neurotubules was the same as that in the controls on day 1, but thereafter progressively decreased, and they had almost disappeared by day 5. Schwann cells began to migrate from the proximal stump of the transected nerve on day 3, showing their strong effect in promoting the axonal elongation. The initial acceleration of the growth seemed to be induced by the unusual mass of neurofilaments, and the suppression of growth at and after day 3 might be the result of both the decrease in the number of neurotubules and a refractory state of the axons to the stimuli from the migratory Schwann cells.

Acrylamide↗

PubMed1992

Synthesis of allyl 6-O-(3-deoxy-alpha- and -beta-D-manno-oct-2- ulopyranosylonic acid)-(1----6)-2-deoxy-2-[(3R)-3-hydroxytetradecanamido]- beta-D-glucopyranoside 4-phosphate and of the copolymer of the alpha anomer with acrylamide.

The title disaccharides were synthesized by mercuric cyanide-catalyzed condensation of methyl (4,5,7,8-tetra-O-acetyl-3-deoxy-alpha-D-manno-oct-2-ulopyranosyl bromide)onate and allyl 2-[(3R)-3-acetoxy-tetradecanamido]-3-O-benzyl-2-deoxy-beta-D- glucopyranoside, followed by phosphorylation of the alcoholic function of the amino sugar. The phosphorylated anomers were separated by chromatography and deprotected by conventional methods. Polymeric material was obtained by copolymerisation, catalyzed by peroxosulphate and N,N,N',N'-tetramethylethylenediamine, of the alpha anomer with acrylamide; it contained ca. one disaccharide unit for 18 acrylamide residues.

Acrylamide↗

PubMed1993

Acrylamide quenching of the intrinsic fluorescence of tryptophan residues genetically engineered into the soluble colicin E1 channel peptide. Structural characterization of the insertion-competent state.

Colicin E1 or any of its COOH-terminal channel peptides can be activated in vitro by acidic (< 4.5) pH or detergents. In its activated or insertion-competent state, the colicin E1 thermolytic (178 residue) channel peptide demonstrated an increased ability to bind and form channels in artificial membranes. An earlier report [Merrill et al. (1990) Biochemistry 29, 5829-5836] indicated that the structural change occurring in the channel peptide upon activation was not a large unfolding but seemingly involves a more subtle conformational change. To probe the solution structure of the colicin channel peptide and the structural changes occurring upon activation, 12 single-tryptophan-containing mutant peptides have been prepared. All of the peptides displayed cellular cytotoxicity comparable to the wild-type peptide. Fluorescence quenching by acrylamide of each Trp residue genetically engineered into the channel peptide indicated that tryptophyls located at positions 355, 367, 393, 413, and 443 report significant conformational changes which are associated with the insertion-competent state. Calculation of the bimolecular quenching constants for each single-Trp peptide showed that there are three classes of Trp residues found in the native colicin E1 channel peptide. None of the Trp residues were found to be completely inaccessible to acrylamide (buried). The NH2-terminal region near Trp-355 and -367 along with the COOH-terminal hydrophobic domain, including Trp-484, -495, and -507, was largely buried in the channel peptide soluble structure. Two peptide segments, one containing Trp-393, -404, and -413 and a second encompassing Trp-431 and -443, were moderately to very exposed regions in the soluble channel peptide.(ABSTRACT TRUNCATED AT 250 WORDS)

Acrylamide↗

PubMed1984

Tryptophan emission from myosin subfragment 1: acrylamide and nucleotide effect monitored by decay-associated spectra.

The intrinsic emission due to the tryptophan residues of the heavy chain of myosin subfragment 1 can be divided into three classes, on the basis of spectra associated with lifetimes of 0.72, 4.5, and 8.8 ns. The percentage contribution of each component to the total emission is 9%, 45%, and 46%, respectively. Low concentrations of acrylamide quench the long component with a quenching constant of 14.9 +/- 2.9 M-1, while the intermediate and short components are unaffected. Upon addition of ATP the total intensity increases by 17%. The bulk of this increase is in the intermediate lifetime component. Quenching by acrylamide in the presence of ATP again quenches only the long lifetime component, indicating that the tryptophan residues affected by ATP binding are not accessible to the solvent.

Acrylamide↗

PubMedDate not supplied

Solvent-free vapor-phase photografting of acrylamide onto poly(ethylene terephthalate).

Poly(ethylene terphthalate) (PET) films were photografted under reduced pressure in a solvent-free vapor of acrylamide and a co-initiator, benzophenone. Characterization of grafted samples by ESCA and contact angles showed that the grafting increased with grafting time and temperature. The amide groups obtained by the acrylamide grafting were converted into amine groups by the Hofmann rearrangement to be used in coupling reactions. The amine groups were confirmed by reaction with pentafluorobenzoyl chloride, which provides a fluorine label for ESCA. Surface grafting of polymeric substrates in the vapor phase induced by plasma or high energy and UV irradiation is reviewed.

Acrylamide↗