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PubMed1985

Uptake, disposition, and elimination of acrylamide in rainbow trout.

The uptake, disposition, and elimination of [2,3-14C]acrylamide was studied in fingerling rainbow trout exposed to 0.388 and 0.710 mg/liter [2,3-14C]acrylamide at 12 degrees C under static water conditions for 72 hr. 14C in carcass and viscera was determined at times ranging from 4 to 72 hr after the beginning of the exposure period and 4 to 96 hr after transfer of the fish to fresh flowing water for the elimination studies. Uptake of 14C was initially rapid and plateaued after 72 hr of acrylamide exposure. No appreciable bioaccumulation occurred in carcass or viscera at either exposure concentration and 14C distributed approximately equally to all tissues studied. Elimination of 14C from carcass and viscera was biphasic with a terminal half-life of approximately 7 days. 14C elimination was not uniform in all tissues studied with the most rapid elimination occurring in blood and gill and the slowest elimination occurring in muscle and intestine. In addition, 10 to 15% of the initial total 14C in carcass or viscera was nonextractable and was associated with the protein fraction of the sample at all time points in the depuration period. Approximately 20% of an ip administered dose of [14C]acrylamide was eliminated via the gills, 7% via the urine, and less than 1% via the bile in 2 hr. At least three biliary metabolites were isolated by HPLC.

Acrylamide↗

PubMed1985

Distribution and binding of [14C]acrylamide to macromolecules in SENCAR and BALB/c mice following oral and topical administration.

To determine if differences in acrylamide distribution or its binding to DNA could be responsible for the reported higher incidence of skin papillomas observed after oral administration compared to topical application, [14C]acrylamide was administered by topical application and oral intubation to male SENCAR and BALB/mice. Portions of lung, liver, stomach, testes, and skin were removed, and 14C was measured at 15 min, 30 min, 1, 6, 12, 24, and 48 hr. Binding to DNA, RNA, and protein was measured at 6 and 48 hr. Following oral administration, few strain differences in distribution or binding were noted. After topical application, SENCAR mice generally showed higher tissue concentrations than did the BALB/c mice at the early time periods but not at the later ones. Comparing the two routes, comparable concentrations were observed in all tissues except the skin where the amount of [14C]acrylamide after topical application was approximately 100 times that observed after oral administration. At 48 hr, binding to DNA was sevenfold higher after topical than after oral administration. The effect of route on papilloma formation cannot be explained, therefore, on the basis of either a difference in distribution or binding to DNA in the target organ. The binding of acrylamide to DNA in skin was similar in both SENCAR and BALB/c mice indicating that the much greater susceptibility of the SENCAR mice to tumorigenesis cannot be explained simply on the basis of distribution or macromolecular binding.

Acrylamide↗

PubMed1986

The distribution of [14C]acrylamide in male and pregnant Swiss-Webster mice studied by whole-body autoradiography.

Male and 13.5- and 17.5-day pregnant Swiss-Webster mice were administered 120 mg/kg [2,3-14C]acrylamide orally. The male mice were frozen 0.33, 1, 3, 9, 24, 72, and 216 hr later, and the pregnant mice at each gestational period were frozen at 3 and 24 hr. Whole-body autoradiographs from the male mice at early time intervals revealed accumulation of radioactivity in the contents of the gastrointestinal tract, liver, pancreas, testis, brain and gallbladder, and epithelia of oral cavity, esophagus, and bronchi. The distribution appears to be similar in the male and pregnant mice. Absorption from the stomach was virtually complete by 3 hr; renal and hepatic elimination was essentially complete at 24 hr. Radioactivity in the male reproductive tract appeared in the parenchyma of the testis at 1 hr, moved to the seminiferous tubules and head of the epididymis at 9 hr, and by 9 days remained only in the tail of the epididymis and the crypts of the epithelium of the glans penis. This movement parallels that of spermatids. The 13.5-day fetuses were uniformly labeled except for a slightly increased uptake in fetal brain. The distribution of radioactivity in the 17.5-day fetal tissues resembled that in maternal tissues; the remarkable exception was an intense accumulation in fetal skin. This study indicates that acrylamide is efficiently absorbed from the stomach and eliminated by the liver, kidney, and possibly the pancreas. A previously unrecognized affinity of acrylamide or a metabolic product was demonstrated for fetal skin in late gestation and for adult epithelia of oral cavity, esophagus, forestomach, and bronchi. Also, acrylamide or a metabolite appears to bind to spermatids at a specific stage near maturation.

Acrylamide↗

PubMed1987

Behavioral and histological effects of acrylamide in rainbow trout.

A histological and behavioral study was used to assess whether acrylamide produced neurotoxic effects in rainbow trout. Swimming performance of trout exposed to 0, 12.5, or 25 mg/liter acrylamide for 15 days was unaffected. Swimming performance of animals exposed to 50 mg/liter acrylamide for a similar time period was compromised by morbidity and mortality of the animals in this treatment group. The absence of dose-related histological lesions in central neurons, peripheral neurons or muscle suggested that the observed deficit in swimming performance was due to a generalized toxic response. Acrylamide treatment produced dose-related lesions in the gill and liver of rainbow trout.

Acrylamide↗

PubMed1990

Synaptic terminal degeneration and remodeling at the rat neuromuscular junction resulting from a single exposure to acrylamide.

Repetitive exposure to low doses of acrylamide results in extensive pathological changes at the neuromuscular junction (NMJ), but it remains undetermined if a single exposure to a larger dose will produce a similar neuropathological outcome. In the present study, morphometric and ultrastructural analyses of rat soleus NMJ were performed to determine early pathological effects of an intraperitoneal injection of 100 mg/kg acrylamide. Widespread nerve terminal degeneration, terminal sprouting, and endplate lengthening were evident as early as 4 days after injection. Degenerating terminal branches were swollen and exhibited enhanced argyrophilia. Ultrastructurally, the majority of terminals exhibited axolemmal abnormalities, neurofilament accumulations, and a paucity of synaptic vesicles; occasional swollen terminals lacked neurofilaments but contained increased numbers of tubulovesicular profiles. This early morphological pattern of nerve terminal changes suggests that acrylamide may disrupt both synaptic vesicle recycling and neurofilament degradation. These findings indicate that a single high dose of acrylamide triggers pathological lesions and remodeling in motor nerve terminals virtually identical to those resulting from multiple low doses.

Acrylamide↗

PubMed1993

Bench-scale production of acrylamide using the resting cells of Brevibacterium sp. CH2 in a fed-batch reactor.

Effects of various organic acids and salts on the stabilization of nitrile hydratase were investigated. The stability of the nitrile hydratase of Brevibacterium CH2 during storage was greatly enhanced by the addition of n-butyric acid. Effects of temperature, pH, and concentrations of acrylonitrile and n-butyric acid on acrylamide production by the resting cells were also investigated. Acrylamide production per unit dry weight of the cells increased 1.33 times by the addition of 0.05% n-butyric acid. A 20% acrylamide solution was successfully produced in a bench-scale reactor (12 l) with only a trace amount of salts after 10 h of hydration reaction under optimum reaction conditions without using an isotonic substrate. The conversion yield was nearly 100%, and acrylic acid as a by-product was not produced. Final acrylamide production of 400 g g-1 cells and productivity of 20 g/(g cells l-1 x h-1) were obtained.

Acrylamide↗

PubMed1988

Clastogenic effects of acrylamide in mouse bone marrow cells.

Acrylamide, known to induce dominant-lethal mutations (Shelby et al., 1986; Smith et al., 1986) and heritable translocations (Shelby et al., 1987) in rodent germ cells, was hitherto a questionable clastogen in rodent bone marrow (Shiraishi, 1978). Therefore, it was tested for chromosomal aberrations in mouse bone marrow cells, spermatogonia and by the micronucleus test. The intraperitoneally injected doses ranged from 50 to 150 mg/kg. In the chromosomal bone marrow test and the micronucleus assay positive results were obtained with acrylamide, and in the latter test the effect increased linearly with dose. Chromosomal aberrations were not induced in differentiating spermatogonia by the acute acrylamide treatment. Cisplatin was used as a positive control and gave the expected positive response in all 3 tests. The present results demonstrate that acrylamide is no exception among clastogens. It breaks chromosomes not only in mammalian germ cells but also in somatic cells.

Acrylamide↗

PubMed1984

Neurotoxic effects of acrylamide on rat retinogeniculate fibres.

The common laboratory chemical, acrylamide, causes various clinical effects including dysfunction of the visual system. Previous electrophysiological recordings from the rat lateral geniculate nucleus (LGN) following exposure to acrylamide suggested that X-like cells were selectively disrupted by the neurotoxin. This study examines the possibility that the diameter of the optic tract fibres may underlie their differential susceptibility, but shows that fibres of all sizes are affected by acrylamide intoxication and the results suggest that the selective effect of acrylamide is not due simply to disruption of optic tract fibres.

Acrylamide↗

PubMed1986

The association of acrylamide with proteins. The interpretation of fluorescence quenching experiments.

The association properties of acrylamide with a number of proteins in aqueous solution have been investigated by a fluorescence-quenching method previously used in micelles and lipid bilayers (Blatt, E., Chatelier, R.C. and Sawyer, W.H. (1984) Chem. Phys. Lett. 108, 397-400). At pH 7.0, acrylamide partitions between the bulk aqueous phase and the proteins, human serum albumin, monellin and ovalbumin. Comparison with an earlier method of analysis (Sikaris, K.A., Thulborn, K.A. and Sawyer, W.H. (1981) Chem. Phys. Lipids 29, 23-36) confirms the data quantitatively. For human serum albumin at pH 2.2, acrylamide associates according to both partition and binding processes. Equilibrium dialysis experiments performed for the latter system verify that acrylamide associates with proteins.

Acrylamide↗

PubMed1987

Does the fluorescence quencher acrylamide bind to proteins?

We have studied the protein concentration dependence of the acrylamide quenching of the fluorescence of the proteins, human serum albumin and monellin, and we have found no such dependence for the concentration range of 0.5-20 mg/ml. These quenching studies were performed by fluorescence lifetime measurements using phase/modulation fluorometry. We have also performed equilibrium dialysis studies, which show no large degree of association of acrylamide with serum albumin, and we have found that acrylamide has only a small effect on the activity of selected enzymes. These various studies do not indicate the existence of strong acrylamide-protein interactions and are in discord with a recent report by Blatt et al. in this journal (Blatt, E., Husain, A. and Sawyer, W.H. (1986) Biochim. Biophys. Acta 871, 6-13).

Acrylamide↗

PubMed1985

Maternal-foetal distribution studies in late pregnancy. II. Distribution of [1-14C]acrylamide in tissues of beagle dogs and miniature pigs.

[carbonyl-14C]Acrylamide was administered iv as a single dose (5 mg/kg) to pregnant beagle dogs and miniature pigs late in gestation. After a 2-hr equilibration period, the animals were killed and foetuses were removed for determination of the amount of radioactivity in maternal and foetal tissues. In total, six dog litters (33 foetuses) and seven pig litters (45 foetuses) were examined. In dogs, acrylamide was distributed readily to both maternal and foetal tissues with a placental distribution factor of 17.7%. The blood/brain distribution factor was insignificant (5.9%) in maternal dogs and 0% in the foetuses. Maternal liver was the largest depot of the administered acrylamide in the dog, followed by the maternal kidney. In pigs, the placental distribution factor was 31%, and the blood/brain distribution factor was insignificant in both maternal and foetal pigs. Liver and kidney of maternal pigs also contained the greatest amount of radioactivity. Although there appears to be some placental protection of the foetuses from the xenobiotic in the maternal circulation, foetal brain would be exposed to the effect of any acrylamide present in the foetal circulation, since the foetuses of both species had blood/brain distribution factors that were either small or zero, reflecting the absence of a blood-brain barrier.

Acrylamide↗

PubMed1985

Acrylamide neuropathy in the rat: effects on energy metabolism in sciatic nerve.

Energy metabolism was examined in rat sciatic nerve before and after induction of neuropathy by treatment with acrylamide monomer. The in vivo activities of two glycolytic enzymes, glyceraldehyde-3-phosphate dehydrogenase and nerve-specific enolase, were resistant to acrylamide. The levels of adenosine 5'-triphosphate and creatine phosphate were also unaffected by acrylamide after either short-term or long-term treatment. The turnover of high-energy phosphate was somewhat reduced in the nerves of severely intoxicated animals. These findings cast doubt on the hypothesis that acrylamide neuropathy begins with an attack on the means of generating metabolic energy, although the eventual failure of one or more energy-consuming processes in peripheral nerve remains likely.

Acrylamide↗

PubMed2001

Environmental risk assessment of acrylamide and methylolacrylamide from a grouting agent used in the tunnel construction of Romeriksporten, Norway.

Increased focus on the possible evironmental risk associated with large-scale use of grouting agents has revealed that leakage of chemicals from grouting activities may cause harm to the environment. Chemical grouting agents are used to reduce water leakages in e.g. tunnel constructions. The present study focuses on monitoring results and environmental risk caused by releases of non-polymerised monomers during use of the acrylamide-based grouting agent Rhoca-Gil (Siprogel). Drainage water from the tunnel Romeriksporten was monitored with respect to acrylamide and methylolacrylamide, as leakage of these substances was observed earlier in connection with similar constructions where Rhoca-Gil was used. Concentrations of acrylamide and methylolacrylamide in the draining water showed that these substances leaked out both in connection with the injection of Rhoca-Gil and in connection with after-injection using other grouting agents. Gel formation studies with Rhoca-Gil showed that a low degree of polymerisation (and hence, large leakages of monomers) can be expected if the product is diluted with water. Results from investigation of the environmental fate of methylolacrylamide showed that this substance is chemically transformed at the high-pH conditions of the tunnel. Ecotoxicological testing of the substances and an environmental effects assessment for the receiving water (River Alna and the Oslofjord) showed that the discharge of acrylamide and methylolacrylamide may have caused effects on the aquatic life in the river and in a limited area of the fjord.

Acrylamide↗

PubMed1996

Induction of hypoploidy and cell cycle delay by acrylamide in somatic and germinal cells of male mice.

Monomeric acrylamide was tested for its potential to induce aneuploidy in spermatocytes and bone marrow cells of mice. For this purpose, chromosomes from metaphase spreads were counted semi-automatically. In both test systems, cell proliferation was monitored, determining the meiotic index of spermatocytes and the average generation time of bone marrow cells after BrdU incorporation, respectively. No indications could be seen for different sensitivity of somatic and germinal cells towards acrylamide. With a dose of 120 mg/kg, the chemical caused cell cycle delay in both germ line and somatic cells. There was diverging response with respect to the balance of hypo- and hyperploidy. While the percentage of chromosome loss was significantly elevated in both test systems, acrylamide treatment did not increase the frequency of hyperploid cells. Interpreting these results on the basis of conventional test protocols, acrylamide should not be considered as an aneugen. The conservative approach, however, may be inadequate for the detection of aneugenic mechanisms different from non-disjunction.

Acrylamide↗

PubMed1991

Inhibition of substrate binding to the adrenal cytochrome P450C-21 by acrylamide and its implications for solvent accessibility of the binding site in the microsomes.

The present study offers evidence indicating that acrylamide, a highly polar molecule and an efficient quencher of tryptophanyl fluorescence, inhibits substrate binding to P450C-21 in bovine adrenocortical microsomes, in a competitive manner similar to that in the purified enzyme. Resolution of the fluorescence-quenching data revealed an acrylamide quenching constant (K2 = 9.9 M, that is, the association constant for the quencher-fluorophore complex) that was similar to the reciprocal of its inhibition constant (1/Ki = Ka = 8.3 +/- 0.9 M) for substrate binding. The substrate inhibited the fluorescence quenching by acrylamide as indicated by its concentration-dependent decrease in K2. The inhibition was in accordance with partial competition. These results are essentially similar to those previously observed in the purified lipid-free enzyme. In addition, the substrate dissociation, acrylamide inhibition, and fluorescence-quenching constants and the tryptophanyl fluorescence maximum (340-342 nm) were essentially the same in the microsomes and the lipid-free purified enzyme. These results indicate that the substrate-binding site of P450C-21 and the concerned tryptophan are accessible to the highly polar molecule in the microsomal membranes, similar to that in the lipid-free purified enzyme. This implies that the substrate-binding site is not shielded by lipids in such a way that only the substrate in the lipid phase can gain access to the binding site. This conclusion is consistent with the currently favored model, for membrane topology of mammalian P450 enzymes, in which P450 is anchored to the membrane through a short N-terminal sequence while the remaining portion of the molecule is exposed to polar environment.

17-alpha-Hydroxyprogesterone↗

PubMed1983

A study of the quenching of the intrinsic fluorescence of succinyl-CoA synthetase from Escherichia coli by acrylamide, iodide, and coenzyme A.

Escherichia coli succinyl-CoA synthetase (SCS) contains three tryptophan residues per mole of alpha beta dimer, and all of them are on the beta subunit. SCS shows an emission maximum at 335 nm which is shifted to 350 nm upon denaturation by urea or guanidine hydrochloride. Acrylamide is able to quench the tryptophan fluorescence in SCS by static and dynamic mechanisms. Substrates give protection against quenching by acrylamide. Binding of ATP to the alpha subunit which has no tryptophans gives as large an effect on the quenching by acrylamide as the binding of coenzyme A (CoA) to the beta subunit. Addition of CoA eliminates the curvature observed in Stern-Volmer plots for acrylamide quenching obtained by lifetime measurements. Potassium iodide does not quench the SCS fluorescence in the presence of CoA. These results suggest that there are heterogeneously emitting tryptophan residues in SCS that are located at the alpha beta subunit contact region close to the CoA binding site. Hence, the tryptophan residues can act as intrinsic reporters of events taking place at the active site of this enzyme. Further, the present results support models for SCS that put the active site at the alpha beta subunit contact region.

Acrylamide↗

PubMed1992

Protein malnourishment: a predisposing factor in acrylamide toxicity in pregnant rats.

Exposure to acrylamide (3-10 mg/kg body weight) was found to be lethal for protein-deficient pregnant rats as evidenced by their increased mortality. It had no such effect on the normal protein diet fed pregnant and nonpregnant rats and the protein-malnourished nonpregnant rats. Protein deficiency during pregnancy caused a significant decrease in the activity of brain monoamine oxidase and acetylcholinesterase and striatal [3H]spiperone binding, known to label dopamine receptors; had no significant effect on the binding of 3H-QNB (quinuclidinyl benzilate) to cerebellar and [3H]diazepam to frontocortical membranes, known to label muscarinic and benzodiazepine receptors, respectively; and had no significant effect on brain glutathione (GSH) levels in comparison with pregnant rats fed normal protein diet. Exposure to acrylamide (2 mg/kg body weight) in protein-malnourished pregnant rats caused a marked decrease in the activity of monoamine oxidase and acetylcholinesterase and also in the binding of [3H]spiperone, [3H]QNB, and [3H]diazepam to striatal, cerebellar, and frontocortical membranes, respectively. Kinetic studies revealed that decreased binding of these ligands in the specific brain regions were due to decreased receptor sites (Bmax). A reduction in the brain glutathione content was also observed in these animals in comparison with those fed a low-protein diet during pregnancy. Pregnant rats fed a normal-protein diet on acrylamide exposure, however, showed no such biochemical changes in comparison with the pregnant rats fed normal protein diet. Also, no effect on any of the parameters studied was observed in the adult nonpregnant rats fed a low-protein diet (for 18 d) and those exposed to the monomer (d 6-17) fed either a normal- or low-protein diet in comparison with respective controls. The results indicate that pregnancy under conditions of malnutrition modifies the susceptibility of pregnant rats toward acrylamide.

Acetylcholinesterase↗

PubMed1995

Acrylamide arrests mitosis and prevents chromosome migration in the absence of changes in spindle microtubules.

Cultured HT 1080 fibrosarcoma cells were exposed to acrylamide (ACR), an industrial neurotoxicant that disrupts neuronal intracellular transport, to determine if mitosis (another microtubule-based intracellular transport system) was adversely affected. The number of cells arrested in mitosis increased, in a concentration-dependent manner, from 1 to 10 mM acrylamide. A 4-h exposure to 10 mM acrylamide increased the mitotic index by 4.5-fold over control, comparable to the arrest caused by colchicine. In mitotic acrylamide-exposed cells, the chromosomes remained at the metaphase plate; no changes in spindle microtubules (MTs), as seen with tubulin immunofluorescence, were observed. The distance between spindle poles (interaster) was the same in control and experimental cells. The non-neurotoxic analogue methylene bisacrylamide had no effect in the same concentration range. The data suggest potential molecular mechanisms of action for general toxicity and neurotoxicity to be disruption in MT disassembly or MT-kinetochore interactions and/or cellular homeostasis.

Acrylamide↗