SEARCH · PubMed Health

Results for “Acrylamides”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 523 records · Page 29Linked to original sources

PubMedDate not supplied

The neurotoxins 2,5-hexanedione and acrylamide promote aggregation of intermediate filaments in cultured fibroblasts.

Axonal swellings associated with large aggregates of neurofilaments are characteristic of neuropathies caused by chemical neurotoxins (n-hexane, methyl n-butyl ketone, and acrylamide) or giant axonal neuropathy (GAN--an autosomal recessive genetic disease). In GAN, filamentous aggregates have been shown also to occur in other cell types including cultured skin fibroblasts. Therefore, we studied the effects of 2,5-hexanedione (the neurotoxic metabolite of n-hexane and methyl n-butyl ketone) and acrylamide on normal human skin fibroblasts in tissue culture. We show that both neurotoxins induce aggregation of intermediate filaments of the vimentin type in the cultured fibroblasts without disrupting microtubules.

Acrylamide↗

PubMed1993

Axonal sprouting of motor nerve in acrylamide-intoxicated rats with progressive weakness.

Quantitative morphologic studies on the motor axons in endplates of extensor digitorum longus muscle (EDL M) and soleus muscle, and on the myelinated fibers of the nerve to EDL M and other lower limb nerves were made on rats showing progressive weakness, intoxicated with acrylamide for 4 weeks (test), using silver staining. Terminal sproutings were significantly greater in frequencies in test compared with control in both muscles. In addition, morphologic changes in test consisted of a significant increase in the number of axon terminal branches and in the frequency of swellings of the preterminal, terminal, and ultraterminal axons and in an increase of myelinated fibers showing axonal degeneration in the nerve to EDL M. Such findings were in contrast with the previous report that cumulative doses of acrylamide inhibit sprouting of motor axons in endplates.

Acrylamide↗

PubMed2005

Some analytical factors affecting measured levels of acrylamide in food products.

Acrylamide in food is normally measured as "free water-soluble acrylamide". However, it is shown that certain extraction techniques, like extraction as for dietary fibre or at high pH can affect the result. This has to be accounted for, particularly in exposure assessment and in studies of bioavailability and, in the long run, the health risk assessment.

Acrylamide↗

PubMed1994

The volume of Purkinje cells decreases in the cerebellum of acrylamide-intoxicated rats, but no cells are lost.

The effects of acrylamide intoxication on the numbers of granule and Purkinje cells and the volume of Purkinje cell perikarya have been evaluated with stereological methods. The analysis was carried out in the cerebella of rats that had received a dose of 33.3 mg/kg acrylamide, twice a week, for 7.5 weeks. The total numbers of cerebellar granule and Purkinje cells were estimated using the optical fractionator and the mean volume of the Purkinje cell perikarya was estimated with the vertical rotator technique. The volumes of the molecular layer, the granular cell layer and the white matter were estimated using the Cavalieri principle. The mean weight of the cerebellum of the intoxicated rats was 7% lower than that of the control rats (2P = 0.001). The numbers of the Purkinje cells and granule cells were the same in both groups, but the mean volume of the perikarya of the Purkinje cells in the intoxicated rats was 10.5% less than that of the control group (2P = 0.004). The volume of the granular cell layer was reduced by 15% (2P = 0.006) but there were no differences in the volumes of the molecular layer and the white matter in the intoxicated and control animals.

Acrylamide↗

PubMed1993

Quantitative measurements of vibration threshold in healthy adults and acrylamide workers.

The early detection of impaired vibration sensation is necessary in order to monitor the adverse effects in workers occupationally exposed to neurotoxic chemicals such as acrylamide. The conventional neurological examination which assesses vibration sensation by utilizing a tuning fork is relatively insensitive for this purpose. In the present study, the Vibration II, a new device for the quantitative measurement of vibration thresholds, was used in 105 healthy Chinese adults. A new testing procedure combining the "two-alternative forced-choice procedure" and the "yes-or-no method-of-limits procedure" showed good reliability and was less time consuming. The results indicate that significant differences in the vibration threshold of index fingers and great toes were found neither between males and females, nor between the left and the right side. However, there was an age-dependent increase in vibration threshold in nonexposed healthy subjects. The vibration thresholds of 41 workers exposed to acrylamide detected by the Vibration II were significantly higher than those of the healthy adults in the same age group. The quantitative measurement of vibration threshold seems to be potentially useful for screening peripheral nerve dysfunction in field studies.

Acrylamide↗

PubMed1994

Attenuation of glyceraldehyde-3-phosphate dehydrogenase activity and ATP levels in rat brain synaptosomes by acrylamide.

The effect of neurotoxin acrylamide (AC) on energy metabolism has been studied in a purified preparation of the synaptosomes. The synaptosomes were prepared by the flotation technique in a discontinuous Ficoll/sucrose gradient. The purity of the synaptosomes was checked by electron microscopy and by assaying the activity of marker enzymes. By these criterias, free mitochondrial contamination in the synaptosomes was found to be > 2%. Incubation of the synaptosomes with different concentrations of AC (2.5, 5.0, and 10mM) produced a concentration-dependent inhibition (15, 35, and 60%, respectively) of glyceraldehyde-3-phosphate dehydrogenase activity. Acrylamide also produced a time-dependent decrease of ATP concentrations in the synaptosomes; about 25% loss of ATP was seen within 1h, while about 60% ATP was lost after 120 min incubation with 10 mM AC. The effect of known inhibitors of glycolysis-iodoacetic acid (IAA), and of oxidative phophorylation-rotenone and antimycin A, was also studied on ATP synthesis by the synaptosomes. IAA was found to be the most potent inhibitor of ATP synthesis, while both rotenone and antimycin A were equally effective in blocking ATP synthesis in the synaptosomes. These studies show that the synaptosome might be used as a suitable in vitro model to study the effect of neurotoxin such as AC on neuronal energy metabolism.

Acrylamide↗

PubMed1994

Number and volume of rat dorsal root ganglion cells in acrylamide intoxication.

Acrylamide intoxication induces a filamentous neuropathy with breakdown of distal axons and chromatolytic reaction of dorsal root ganglion cells. To obtain quantitative information about the perikaryal alterations neurons of the fifth lumbar dorsal root ganglion of rats were examined with stereological techniques following intoxication with a total dose of 500 mg acrylamide. Number, mean volume and distribution of neuron volume were estimated for each of the two cell subpopulations using optical disectors, the four-way-nucleator and systematic sampling techniques. In intoxicated rats perikaryal volume of A-cells was significantly reduced by 28%, from 63,200 micron3 (CV = 0.16) to 45,500 micron3 (CV = 0.19), whereas the volume of B-cells was unchanged. Numbers of A- and B-cells were preserved. The finding of a selective atrophy of A-cell perikaryal volume is in accordance with previous observations of predominant alterations of large myelinated sensory fibres and most likely reflects an attack on the perikaryal neurofilaments abundant in this cell type.

Acrylamide↗

PubMed1983

Alterations in retinal neurotransmitter receptors and neuropeptides of the chick by kainic acid and acrylamide.

The effects of intraocular injection of kainic acid and acrylamide upon retinal neuropeptides and high affinity binding sites have been determined in the chick. Kainic acid causes a sharp reduction in Met-enkephalin and somatostatin while neurotensin levels are unchanged. This treatment also lowers the extent of cholinergic muscarinic but not of [3H]naloxone or [3H]spiroperidol binding. In contrast, acrylamide treatment causes major increases of retinal Met-enkephalin and neurotensin concentrations. The binding of [3H]naloxone is also increased, and no reductions of any peptide or binding intensity were observed. The results indicate the plasticity of retinal neuropeptide levels and the selectivity with which these can be modulated.

Acrylamide↗

PubMed1987

Nodes of Ranvier in acrylamide neuropathy: voltage clamp and electron microscopic analysis of rat sciatic nerve fibres at proximal levels.

Adult male rats were injected with acrylamide monomer (50 mg/kg i.p., 3 times/week). The animals developed hind limb paresis and distal motor nerve conduction velocity decreased. Three of 14 examined isolated myelinated sciatic nerve fibres showed a reduced excitability. In the remaining fibres the action potentials were normal. Potential clamp analysis of nodes of Ranvier in the single fibres revealed large delayed nodal K currents in 6 cases. Four of these 6 fibres exhibited a markedly increased membrane capacitance and in 2 fibres an increased Na permeability was found. Electron microscopic examination of sciatic nerves revealed comparatively subtle internodal and nodal-paranodal alterations in large myelinated fibres. Internodally, focal aggregates of tubulovesicular profiles could be found and some Schwann cells were hypertrophic. Paranodally, axonal evaginations penetrated in between the terminating myelin lamellae. Some paranodes had a very thin myelin covering and/or exhibited varying degrees of myelin sheath retraction. In the nodal axon domains lacking an axolemmal undercoating and partly non-undercoated axolemmal protrusions could be found. Similar physiological and morphological alterations occur in the rat sciatic nerve above a neuroma. Therefore, the presently observed proximal changes may, to some extent, represent non-specific alterations, secondary to a target deprivation caused by the distal axon degeneration typical for acrylamide neuropathy.

Acrylamide↗

PubMed1988

Histological changes of acrylamide-induced testicular lesions in mice.

The effects of a single oral dose of 150 or 100 mg/kg acrylamide on the testis were studied histopathologically in prepubertal and adult mice over a period of 10 days following treatment. In the prepubertal mice, severe testicular damage such as vacuolation and swelling of the round spermatids, necrosis of the late elongated spermatids in stages I to VIII, abnormal meiosis in stage XIX, and a marked cellular exfoliation into the lumen were detected 1 day after administration of the 150 mg/kg dose. On Day 2, the damage was more pronounced. However, the testicular damage was repaired 7 to 10 days after treatment. In the adults, many tubules from stages I to VIII were affected, showing nuclear vacuolation in most of the round spermatids 1 day after administration of the 150 mg/kg dose. Meiosis in stage XIV was normal. In the prepubertal mice, nuclei of the round spermatids in stage I-III, especially step 1 spermatids had degenerated 1 day after administration of the 100 mg/kg dose. In the adults, the round spermatids had degenerated in stages I-II and IV-VIII 1 day after administration of the 100 mg/kg dose. These results suggested that the most vulnerable cell type among the spermatogenic cells was the round spermatid, especially that in the Golgi phase (stage I-III). Other stages and spermatogenic cells were relatively resistant to acrylamide testicular toxicity.

Acrylamide↗

PubMed1993

Fluorescence quenching at interfaces and the permeation of acrylamide and iodide across phospholipid bilayers.

Studies of fluorescence quenching in membrane proteins are complicated by the fact that the barrier effect of the bilayer towards the quenchers is not known with precision. Our studies show that (a) both acrylamide and iodide can permeate the membrane at comparable rates, (b) when quenchers are added externally to a vesicle suspension, the apparent Stern-Volmer quenching constants for the same fluorophores are lower in the inner than in the outer aqueous compartments, and (c) at least some non-polar fluorophores embedded in the bilayer are quenched by iodide, but not by acrylamide.

Acrylamide↗

PubMed1994

Ultra-high dose methylcobalamin promotes nerve regeneration in experimental acrylamide neuropathy.

Despite intensive searches for therapeutic agents, few substances have been convincingly shown to enhance nerve regeneration in patients with peripheral neuropathies. Recent biochemical evidence suggests that an ultra-high dose of methylcobalamin (methyl-B12) may up-regulate gene transcription and thereby protein synthesis. We examined the effects of ultra-high dose of methyl-B12 on the rate of nerve regeneration in rats with acrylamide neuropathy, using the amplitudes of compound muscle action potentials (CMAPs) after tibial nerve stimulation as an index of the number of regenerating motor fibers. After intoxication with acrylamide, all the rats showed equally decreased CMAP amplitudes. The animals were then divided into 3 groups; rats treated with ultra-high (500 micrograms/kg body weight, intraperitoneally) and low (50 micrograms/kg) doses of methyl-B12, and saline-treated control rats. Those treated with ultra-high dose showed significantly faster CMAP recovery than saline-treated control rats, whereas the low-dose group showed no difference from the control. Morphometric analysis revealed a similar difference in fiber density between these groups. Ultra-high doses of methyl-B12 may be of clinical use for patients with peripheral neuropathies.

Acrylamide↗

PubMed1990

Induction of dominant lethal mutations by combined X-ray-acrylamide treatment in male mice.

The induction of mutations following combined treatment with acrylamide (AA) plus X-rays has been determined using the dominant lethal mutations test in Pzh:SFISS male mice. Combinations of a mutagenic dose of both agents (1.00 Gy, 125 mg/kg b.w.) and a non-mutagenic dose, i.e., a dose that alone does not produce dominant lethals (0.25 Gy, 25 mg/kg b.w.), were used. For the discussion of the effects of combined action of X-rays and acrylamide the term 'enhancement in risk' was used whenever the effects observed after combined exposure significantly exceeded the sum of the effects produced separately by the agents. Such an enhanced risk has been observed in late spermatids after combined action of X-rays and AA at non-mutagenic doses, and in spermatozoa, spermatids and late spermatocytes after exposure to mutagenic doses.

Acrylamide↗

PubMed1994

Increased frequencies of micronuclei in early spermatids of rats following exposure of young primary spermatocytes to acrylamide.

The 'suspension method' for detection of micronuclei in early spermatids (Golgi phase 1 + 2) of rats was used to study induction of chromosomal damage in spermatocytes exposed to single (50 and 100 mg/kg) or fractionated (4 x 50 mg/kg; 24-h intervals) doses of acrylamide. Animals were killed at different time intervals after treatment to measure induction of damage in different stages of spermatocyte development. A statistically significant enhancement of micronucleus frequencies was found after exposure of pre-leptotene spermatocytes to a single dose of 100 mg/kg (days 18 and 20 after treatment) or a fractionated dose of 4 x 50 mg/kg (day 19). In the latter case there was also a significant effect in zygotene spermatocytes that were sampled 15 days after treatment. Comparative studies indicated that the original 'suspension method' can be simplified by omitting enzyme treatments for the release of germ cells from the seminiferous tubules. In the present acrylamide study the old and new procedures gave similar results.

Acrylamide↗

PubMed1994

Dose response for heritable translocations induced by acrylamide in spermatids of mice.

A heritable translocation test was carried out with acrylamide (AA) to obtain a dose-response relationship for induction of reciprocal translocations in late spermatids of the mouse. Male C3H/E1 mice were treated with single i.p. doses of 50 and 100 mg/kg of acrylamide and mated 7-16 days after treatment to untreated female 102/E1 mice. Translocation carriers among the F1 progeny were selected by a sequential procedure of fertility testing and cytogenetic analysis including G-band karyotyping to determine the chromosomes involved in the respective translocations. The translocation frequencies observed with 50 mg/kg and 100 mg/kg of AA were 0.6% and 2.7%, respectively. The historical control translocation frequency was 0.04%. Doubling dose estimates based on these and previous data are discussed.

Acrylamide↗

PubMed1989

Fibronectin network recovery in confluent PtK2 cells after acrylamide treatment.

Confluent PtK2 cells 4 hr treated with 5 mM acrylamide were FN-detected by indirect immunofluorescence. The initial fibrillar-FN network was replaced by an alveolar-type network located at the cell-cell contacts areas in the form of a thick frame with a lace-like appearance. Afterwards, acrylamide removal was obtained by several washes with fresh FCS-free culture medium. Then, PtK2 cells were returned to the incubator for 20 hr. Cell recovery was indicated by reversion of the initial fibrillar-FN network. These data show that FN reversion was possible without any changes in shape and cytoplasmic organization of non-motile growing cells.

Acrylamide↗

PubMed1985

Acrylamide neurotoxicity: altered spinal monosynaptic responses to quipazine, a serotonin agonist, in cats.

The effects of the serotonin agonist quipazine on the spinal monosynaptic reflex (MSR) were investigated in acrylamide-treated cats. Cats were administered 30 mg/kg acrylamide (ACR) for 10 days, and the MSR and spontaneous ventral root discharge (VRD) were recorded on the tenth day (ACR 10) or 10 days subsequent to the last injection (ACR 20). Cumulative doses of quipazine were administered to increase the MSR and VRD. It was found that the MSR in ACR 10 cats was significantly depressed by ACR while the ACR 20 cats showed increased MSRs with double peaks. Dose-response relationships between quipazine and the area-under-the-MSR showed a significant shift to the right in the ACR 10 from control and no significant change in the ACR 20 from control. Dose-response curves of quipazine vs VRD showed no significant difference in either group from control. These data suggest that the alpha-motoneuron in ACR-treated cats was responding normally to quipazine while the primary afferent terminal was not.

Acrylamide↗

PubMed1983

Effects of acrylamide on locomotion and central monoamine function in the rat.

Male rats receiving acrylamide (ACR) in their drinking water (100 ppm) for a six-week period displayed increased psychomotor stimulation to d-amphetamine (d-A; 1.0 mg/kg SC) under several conditions of handling and drug administration. Following behavioral tests a subset of the animals was sacrificed at 15, 50, 80 and 120 minutes following d-A and the brains removed and dissected for determinations of regional brain levels of several monoamine neurotransmitters and metabolites. ACR rats had elevated levels of 5-hydroxyindoleacetic acid (5-HIAA) in the striatum, septal area, and thalamus. The effect was most pronounced at 15 minutes post-drug with ACR rats not demonstrating a depression in 5-HIAA levels present in controls. Increases in accumben's dopamine and norepinephrine levels, evident after d-A, were of lesser magnitude in ACR-exposed rats. Decreases in dihydroxyphenylacetic acid and homovanillic acid, also evident after d-A, persisted for a longer duration in ACR-exposed rats. Light and electron microscopy of spinal cord, striatum, nucleus accumbens and thalamus did not reveal morphologic abnormalities. Sciatic nerves showed histopathological changes characteristic of multi-focal dying-back peripheral nerve degeneration. It was concluded that acrylamide's effect on the psychomotor stimulant properties of d-A may be related to changes in a serotonergic inhibitory system.

Acrylamide↗