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PubMed1979

Screening for neurobehavioral toxicity: the need for and examples of validation of testing procedures.

The need for a sensitive and reliable screen to assess environmental agents for potential behavioral and neurological toxicity is discussed. Factors involving strategy, choice of animals and doses, route of administration, duration of study and requirements for the selection of neurobehavioral tests are also evaluated. The primary emphasis concerns the need for standardization and validation of neurobehavioral tests to be used in neurotoxicology. It is suggested that test validation be accomplished by comparing the observed results of known neurotoxicants in animal models which are chosen to predict effects based on reported human symptomatology. As a means of demonstrating how test validation is used in our laboratory, data from a number of experiments concerning the effects of a variety of chemical agents on three measures of motor functioning were discussed. The neurobehavioral effects of acrylamide, and agent known to produce "dying-back" axonopathies, were assessed using separate techniques presumed to measure hindlimb and forelimb functioning and general motor activity. The prediction that acrylamide will first decrease hindlimb functioning, while decreasing forelimb grip strength and motor activity at higher doses, was confirmed. The validity of the hindlimb measurement was supported using a neurotoxicant, carbon disulfide, known to affect motor functioning in a manner similar to acrylamide. The validity of the forelimb technique was shown indirectly using normative data collected from rats of both sexes tested at various ages, i.e., males were stronger than females and grip scores changed as a function of age. The relative sensitivities of the fore- and hindlimb measurements were found to be approximately the same when used to assess the effects of known muscle relaxants, such as phenobarbital and chlordiazepoxide. Finally, it was predicted and confirmed that an environmental agent believed to affect behavior secondarily to effects on other organ systems would affect all measures of motor functioning at approximately the same dose.

Animals↗
PubMed1971

Serum lipoprotein accumulation in the livers of orotic acid-fed rats.

This study provides confirmation of previous observations that showed that rats fed a diet containing 1% orotic acid for 7 days develop a fatty liver and that there is an inhibition of the secretion of low density lipoproteins without altering general liver protein synthesis. Accumulated fat droplets (liposomes) are entrapped within rough endoplasmic reticulum vesicles. In this study, these vesicles have been shown to accumulate the apolipoproteins of low and very low density lipoproteins. Inhibition of lipoprotein secretion was demonstrated by perfusion of livers from orotic acid-fed rats with a serum-free medium. Liposomes were isolated from these rats. Partially delipidated liposomes, but not similarly treated microsomes or cell sap, were found to form a precipitation line when reacted against anti-low density lipoprotein antiserum. Detergent solubilization of the liposome followed by density gradient centrifugation resulted in a peak at d 1.025 g/ml containing both lipid and protein. Acrylamide electrophoresis in 8 m urea after total delipidation demonstrated liposomal bands which coelectrophoresed with three of four very low density lipoprotein bands; there was no band corresponding to the very low density lipoprotein band which travels furthest in acrylamide electrophoregrams. However, acrylamide electrophoresis of the apoproteins of serum high density lipoprotein from orotic acid-fed animals revealed the presence of the latter band. The results indicate that liver liposomes from orotic acid-fed rats apparently contain the low density apoprotein and probably several other very low density lipoprotein peptides.

Animals↗
PubMed1981

Identification, purification, and radioimmunoassay of NB/70K, a human ovarian tumor-associated antigen.

NB/70K, a tumor-associated antigen of human ovarian epithelial tumor Fraction OCA, has been purified and identified as a glycoprotein which is stable in 0.6 M perchloric acid, binds to concanavalin A, and migrates electrophoretically with alpha-like mobility in barbital-buffered agarose at pH 8.6. NB/70K does not appear to contain normal serum, normal ovary, normal lung, or carcinoembryonic antigen-like cross-reacting antigenic determinants as measured by radioimmunoassay. NB/70K has been purified from ovarian antigen Fraction OCA by chromatography on gamma-globulin coupled to Sepharose 4B and by elution from acrylamide gels. NB/70K migrates as a single band with an apparent molecular weight of 70,000 in sodium dodecyl sulfate:acrylamide gel electrophoresis. A rabbit antibody raised against NB/70K was able to precipitate a polypeptide with a molecular weight of 70,000 as visualized by autoradiography of sodium dodecyl sulfate:acrylamide gels. A radioimmunoassay has been developed for measuring NB/70K activity, using Staphylococcus aureus protein A as a precipitating agent.

Antibodies, Neoplasm↗
PubMed1982

Polyacrylamide-bismuth for postmortem coronary arteriography.

High quality postmortem human coronary arteriograms are obtained by injecting an acrylamide-bismuth mixture into the isolated aortic root under physiologic pressure. The acrylamide advances to the terminal size (20 micrometer.) arterioles, polymerizes, and remains within the vessels during the processing of tissue for histologic studies. Because the polyacrylamide does not affect the arterial wall morphology or the surrounding myocardium, the acrylamide-bismuth injection technique offers the clarity of the cast-corrosion procedure for postmortem radiograms fo the epicardial and intramural coronary arteries and adds the capability for histologic studies of arterial and myocardial tissues.

Acrylic Resins↗
PubMed1996

Fluorescence quenching studies of the rat ovarian LH/hCG receptor.

Fluorescence quenching method providing information about the structure and dynamics of proteins, ligand-protein and protein-lipid interactions was used in a study of the rat ovarian LH/hCG receptor. The efficiency of two different quenchers, acrylamide and iodide, was tested. Acrylamide was significantly more effective in quenching of intrinsic fluorescence of ovarian membranes than iodide and therefore it was used in all of the following experiments. Both acrylamide and iodide were not effective in quenching of membranes labelled with fluorescence probe 1,6-diphenyl-1,3,5-hexatriene (DPH). In the process of desensitization of ovarian LH/hCG receptors the administration to rats of hCG modified the quenching rate of protein fluorescence and intrinsic fluorescence spectral properties of membranes. Alteration in the quenching of intrinsic fluorescence of ovarian membranes was observed after chemical modification of LH/hCG receptors by 2-hydroxy-5-nitrobenzyl bromide (HNB-Br). The accessibility of tryptophan fluorophores was increased in HNB-Br-treated membranes. Delipidation of the LH/hCG receptor modified the quenching of protein fluorescence characteristic for control proteoliposomes. These results demonstrate that fluorescence quenching technique can be successfully applied in the study of the LH/hCG receptor.

Animals↗
PubMed1989

Delayed onset of distal axonal neuropathy in primates after prolonged low-level administration of a neurotoxin.

Short-latency somatosensory evoked potentials were recorded from surface electrodes overlying peripheral nerve, spinal cord, and cortex in 4 monkeys during prolonged intoxication with low levels of acrylamide. A fifth animal served as a longitudinal control subject. Slowing of the response across the spinal-medullary junction was a reliable sign, manifest only after prolonged exposure. Associated morphological changes were preterminal accumulation of axonal neurofilaments without synaptic disruption in the gracile nucleus. The induced alterations in the latency of short-latency somatosensory evoked potentials and in axon morphology were reversible after 7 months of recovery. The extreme delay in onset of subtle neurological dysfunction (940 days) following administration of a presumed safe level of acrylamide suggests that permissible levels of human exposure to toxins of this type should be reassessed.

Acrylamide↗
PubMed1990

Cytoskeletal dynamics in rabbit synovial fibroblasts: II. Reformation of stress fibers in cells rounded by treatment with collagenase-inducing agents.

Modulation of the synthesis and secretion of extracellular matrix proteins and matrix-degrading metalloproteases by rabbit synovial fibroblasts is an important model system for studying the control of tissue-specific gene expression. Induction of collagenase expression is correlated with changes in cell shape and actin filament distribution, but the role of the cellular cytoskeleton in the sustained synthesis and secretion of metalloproteases has not been closely examined. When cells were allowed to respread after rounding by trypsin or cytochalasin, two known metalloprotease inducers, reformation of stress fibers was observed within 2 h in the presence of serum. In the absence of serum, trypsin-treated cells did not respread substantially, even after 24 h in culture. In contrast, cytochalasin-treated cells recovered almost as rapidly in the absence as in the presence of serum, showing reformation of well-formed microfilament bundles within 30 min of drug removal, especially at the spreading cell edges. High resolution electron-microscopic views of detergent-extracted cytoskeletons confirmed the rapid rebundling of peripheral microfilaments. Acrylamide-treated cells fell between these two extremes, spreading slowly in the absence of serum, but almost as rapidly as cytochalasin-treated cells in its presence. Reestablishment of normal intermediate filament distribution generally lagged slightly behind actin for all treatments, and intermediate filaments always appeared to spread back into the cellular cytoplasm within the confines of the reforming peripheral microfilament bundles. No obvious interaction between these two cytoskeletal elements was observed after any treatment, and no specific role for intermediate filaments in modulating gene expression in these cells is suggested by these results. The serum dependence displayed after trypsin or acrylamide treatment may be due to the disturbances in fibronectin synthesis observed in these cells and is consistent with evidence that both induction and sustained expression of matrix-degrading metalloprotease may involve signals transduced through plasma membrane matrix receptors (integrins).

Acrylamide↗
PubMed1995

Concurrent analysis of cytogenetic damage in vivo: a multiple endpoint-multiple tissue approach.

Simultaneous assessment of in vivo micronucleus and chromosome aberration endpoints has been described in the rat and the mouse. Bone marrow and spleen cells were utilized for genotoxicity assessment. A cellulose column methodology was used in the micronucleus assay (where applicable) to eliminate nucleated cells and facilitate cytogenetic scoring. The test agents--cyclophosphamide, chlorambucil, and acrylamide--produced qualitatively comparable results between micronucleus and chromosome aberration endpoints and varied slightly on a quantitative basis depending on the type of test agent and tissue studied. The results from test agents such as cyclophosphamide, chlorambucil, acrylamide, dimethylnitrosamine, vincristine, and x-rays indicated that bone marrow cytogenetic results are similar to spleen and that the spleen tissue is at least as sensitive as the bone marrow. The concurrent analysis of cytogenetic damage in vivo using a multiple endpoint-multiple tissue approach described here has the following advantages: a) reducing the overall animal usage, b) clarifying marginal micronucleus and/or chromosome aberration data, c) correlating cytogenetic results from multiple endpoints and multiple tissues, and d) helping the investigation of the mechanism of action of test agents and their potential target organs. Also, the multiple endpoint-multiple tissue approach can be extended to other endpoints, tissues, and species (where appropriate and practical) to obtain detailed genotoxicity information.

Acrylamide↗
PubMed1991

Synthesis and bioactivity of copolymers with fragments of heparin.

A new type of biocompatible copolymer comprising small fragments of heparin, (octa- to dodecasaccharides) copolymerized with a synthetic monomeric component, viz. acrylamide, has been prepared. The heparin fragments are produced by enzymatic or chemical means and are copolymerized, directly or after suitable derivatization, with acrylamide as the major polymerizable component. The polymeric material incorporates the heparin segments as pendant moieties such that their essential functional groups and structural features for specific binding with the selective serine protease coagulation factor inhibitor antithrombin III are preserved. An important feature of this copolymer is its biocompatibility which relates specifically to its antithrombotic and antithrombogenic activity derived from those of heparin fragments. The biological activity of heparin fragments and copolymers thereof are determined in terms of APTT and anti-Xa activity, their antithrombotic potential being expressed as a ratio of anti-Xa activity to APTT. The copolymers reported have biological activities similar to equivalent amounts of respective heparin fragments, and show higher antithrombotic activity compared to intact heparin or commercially available low-molecular-weight heparin (4,000-6,000 Da).

Acrylamide↗
PubMed1983

Axonal transport in neuropathy.

Recent studies on the distribution of labeled endogenous proteins in the experimental neuropathies induced by streoptozotocin diabetes, galactose feeding, zinc pyridinethione, 2,5-hexanedione, acrylamide, and p-bromophenylacetylurea (BPAU) have demonstrated an impaired build up of retrogradely transported material derived from the more distal parts of peripheral nerve. In BPAU neuropathy the transport abnormality is strongly related to the degree of muscle weakness; following treatment with acrylamide the extent of the impairment is dose related. In both toxic conditions the transport abnormality is present well in advance of the first clinical signs of neuropathy. We therefore suggest that changes in retrograde axonal transport play an initial and important role in the development of many axonopathies.

Acrylamide↗
PubMed1993

Structural determinants of the intrinsic fluorescence emission in notexin and phospholipase A2 enzymes.

Fluorescence measurements of the homologous proteins, notexin and PLA2 enzymes from Naja naja atra, Naja nigricollis, and Hemachatus haemachatus venoms, showed that the wave-length of maximum emission and the quantum yield of their intrinsic fluorescence emission spectra were different. To verify the factors which affected their fluorescence characteristics, the dynamics of tryptophan residues in those homologous proteins were studied by quenching with acrylamide, iodide, and cesium. The degrees of exposure of tryptophanyl groups in notexin and PLA2 enzymes assessed by acrylamide quenching were found to be the major factor that determined their fluorescence characteristics. However, the positively charged groups surrounding tryptophan residues of PLA2 enzymes from N. naja atra and N. nigricollis venoms might affect the quantum yield of their fluorophores. Tryptophan residues of notexin were in an environment with less fluctuation, which did not allow free diffusion of ionic quencher. This might render its tryptophan residues to fluoresce at a shorter wavelength. These results suggested that the structural determinants affecting the intrinsic fluorescence emission of homologous proteins can be easily assessed by quenching studies.

Acrylamide↗
PubMed1996

A fluorescence study of Tn10-encoded tet repressor.

Steady-state fluorescence quenching and time-resolved measurements have been performed to resolve the fluorescence contributions of the two tryptophan residues, W43 and W75, in the subunit of the homodimer of the Tet repressor from Escherichia coli. The W43 residue is localized within the helix-turn-helix structural domain, which is responsible for sequence-specific binding of the Tet repressor to the tet operator. The W75 residue is in the protein matrix near the tetracycline-binding site. The assignment of the two residues has been confirmed by use of single-tryptophan mutants carrying either W43 or W75. The FQRS (fluorescence-quenching-resolved-spectra) method has been used to decompose the total emission spectrum of the wild-type protein into spectral components. The resolved spectra have maxima of fluorescence at 349 and 324 nm for the W43 and W75 residues, respectively. The maxima of the resolved spectra are in excellent agreement with those found using single-tryptophan-containing mutants. The fluorescence decay properties of the wild type as well as of both mutants of Tet repressor have been characterized by carrying out a multitemperature study. The decays of the wild-type Tet repressor and W43-containing mutant can be described as being of double-exponential type. The W75 mutant decay can be described by a Gaussian continuous distribution centered at 5.0 nsec with a bandwidth equal to 1.34 nsec. The quenching experiments have shown the presence of two classes of W43 emission. One of the components, exposed to solvent, has a maximum of fluorescence emission at 355 nm, with the second one at about 334 nm. The red-emitting component can be characterized by bimolecular-quenching rate constant, kq equal to 2.6 x 10(9), 2.8 x 10(9), and 2.0 x 10(9) M-1 sec-1 for acrylamide, iodide, and succinimide, respectively. The bluer component is unquenchable by any of the quenchers used. The W75 residue of the Tet repressor has quenching rate constant equal to 0.85 x 10(9) and 0.28 x 10(9) M-1 sec-1 for acrylamide and succinimide, respectively. These values indicate that the W75 is not deeply buried within the protein matrix. Our results indicate that the Tet repressor can exist in its ground state in two distinct conformational states which differ in the microenvironment of the W43 residue.

Acrylamide↗
PubMed1991

Immobilization of penicillin acylase in porous beads of polyacrylamide gel.

A procedure is described for the immobilization of benzylpenicillin acylase from Escherichia coli within uniformly spherical, porous polyacrylamide gel beads. Aqueous solutions of the enzyme and sodium alginate and of acrylamide monomer, N,N'-methylene-bis-acrylamide, N,N,N,N'-tetramethylethylenediamine (TEMED) and sodium alginate are cooled separately, mixed, and dropped immediately into ice-cold, buffered calcium formate solution, pH 8.5, to give calcium alginate-coated beads. The beads are left for 30-60 min in the cold calcium formate solution for polyacrylamide gel formation. The beads are then treated with a solution of glutaraldehyde and the calcium alginate subsequently leached out with a solution of potassium phosphate. Modification of the native enzyme with glutaraldehyde results in a slight enhancement in the rate of hydrolysis of benzylpenicillin at pH 7.8 and 0.05M substrate concentration. The enzyme entrapped in porous polyacrylamide gel beads shows no measurable diffusional limitation in stirred reactors, catalyzing the hydrolysis of the substrate at a rate comparable to that of the glutaraldehyde-modified native enzyme. The immobilized enzyme preparation has been used in batch mode over 90 cycles without any apparent loss in hydrolytic activity.

Acrylamide↗
PubMedDate not supplied

The same chemicals induce different neurotoxicity when administered in high doses for short term or low doses for long term to rats and dogs.

Dose- and term-dependent differences in the location and nature of brain lesions induced in rats and dogs by 2,5-hexanedione (2,5-HD), misonidazole, clioquinol, and acrylamide are reported. Subchronic neuropathies ("distal axonopathy") were induced by low-dose administration of these neurotoxicants and at high doses, lesions caused by acute or subacute neurotoxicity were found in the central nervous system (CNS). In rats, 2,5-HD induced extracellular edema, nerve cell degeneration, and axonal degeneration in the cerebellar and vestibular nuclei. Similar lesions were observed in misonidazole-treated dogs and clioquinol induced nerve cell degeneration in the hippocampus and malacia in the piriform lobes of these animals. In rats, acrylamide induced degeneration of Purkinje cells. Although the mechanism(s) underlying the differential neurotoxicity of high and low doses of these neurotoxicants remains unclear, we suggest certain biochemical mechanisms, cytotoxic edema and excitotoxicity, as factors in the production of such lesions after high-dose treatment.

Acrylamide↗
PubMed1984

Source and avoidance of the "nothing dehydrogenase" effect, a spurious band produced during polyacrylamide gel electrophoresis of dehydrogenase enzymes from yeasts.

During a study of the distribution of several NAD-linked dehydrogenase enzymes in various yeasts, in which polyacrylamide gel electrophoresis, followed by activity staining with phenazine methosulfate and a tetrazolium was used, a band was frequently detected, the production of which appeared to be independent of any added substrate (the "nothing dehydrogenase" effect). It has been shown that this effect is caused by alcohol dehydrogenase acting on traces of ethanol inadvertently introduced into the system. Two sources of ethanol were identified. They were (i) the enzyme extracts, which could be freed from ethanol by gel filtration, and (ii) the acrylamide used to prepare the gel, which could be freed from ethanol by recrystallization from ethanol-free chloroform. It is suggested that the use of commercial chloroform (stabilized with ethanol) as a recrystallizing solvent is the source of ethanol contamination in commercial preparations of acrylamide.

Acrylamide↗
PubMed1995

In vitro calcium and calmodulin-dependent kinase-mediated phosphorylation of rat brain and spinal cord neurofilament proteins is increased by glycidamide administration.

This study was carried out to determine the action of glycidamide (2,3-epoxy-1-propanamide), a neurotoxic metabolite of acrylamide, on Ca2+/calmodulin (CaM)-dependent protein kinase phosphorylation of cytoskeletal proteins. Acrylamide has been shown to increase Ca2+/CaM-dependent phosphorylation of neurofilament (NF) triplet proteins and autophosphorylation of Ca2+/CaM-dependent protein kinase II (CaM kinase II; EC 2.7.1.37). A daily intraperitoneal dose of 0.7 mmol/kg b.wt. of glycidamide or deionized water was administered to male Sprague-Dawley rats. Animals were sacrificed when signs of severe neurotoxicity became apparent at 13-16 days of treatment. Axonal floatation was used to isolate neurofilaments (NFs) and endogenous kinases from brains and spinal cords of treated and control animals. Samples isolated from brain and spinal cord of glycidamide-treated animals showed increased in vitro Ca2+/CaM-dependent phosphorylation of endogenous and exogenous NF proteins and increased autophosphorylation of CaM kinase II when compared with controls. CaM binding to the alpha, beta, and beta' subunits of CaM kinase II and antibody binding to the alpha-subunit of CaM kinase II in brain supernatant isolates was increased as a result of glycidamide treatment. These results suggest that increased Ca2+/CaM-dependent phosphorylation of cytoskeletal proteins may be involved in the pathogenesis of glycidamide-induced neurotoxicity.

Acrylamide↗
PubMed1983

Relative refractory period as a measure of peripheral nerve neurotoxicity.

A method is presented for converting the relative refractory period to a linear form which can be used for quantifying changes in peripheral nerve conduction and membrane excitability. Since the relative refractory period is very consistent in nerves taken from animals of a given age, strain, and size, small alterations due to exposure by neurotoxic agents can readily be detected. In the present study rat sciatic nerves exposed to phenol developed a peripheral neuropathy which was detected by an increased relative refractory period. Diisopropylfluorophosphate (DFP), another neuropathic agent, produced a shift in the relative refractory period which was also consistent with the time course of its known neurotoxicity. On the other hand, acrylamide did not change the relative refractory period although the rats exhibited deficits when measured behaviorally (roto-rod and inclined screen tests). This observation is consistent with the view that the acrylamide toxicity initially affects nerve endings and spares the nerve axon. Erythrosin B, an agent which enhances nerve excitability, produced a shift in the relative refractory period which indicated that the nerve was less refractory. These examples point to the value of the relative refractory period as an index of the extent and type of neurotoxicity induced by agents which affect peripheral nerve axons, and suggest that this method may be useful in determining the mechanism of action of neurotoxic agents.

Acrylamide↗
PubMed1986

Spatio-temporal vision of macaques with severe loss of P beta retinal ganglion cells.

Anatomical and physiological studies indicate major structural and functional differences between the two parallel retinogeniculate visual pathways in the macaque. We have examined the contribution of these pathways to achromatic visual capacities by behaviorally testing spatio-temporal vision in monkeys with severe damage to the P beta (medium cell) pathway. This loss was produced by systemic administration of a neurotoxicant, acrylamide monomer, a treatment that apparently spares other visual system neurons. Monkeys dosed with acrylamide showed large reductions of contrast sensitivity at high spatial as well as low temporal frequencies. On the other hand, they had normal sensitivity for stimuli of high temporal, low spatial frequency. In addition, dosed monkeys retained normal flicker resolution thresholds for unpatterned stimuli. These findings suggest that the medium cell retinogeniculate pathway contributes primarily to the detection of higher spatial, lower temporal frequencies, while the large cell pathway is involved primarily in sensitivity to lower spatial and higher temporal frequencies.

Acrylamide↗