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At least 19 recordsLinked to original sources

PubMed1979

[Lipoprotein electrophoresis on acrylamide-agarose plates, with discontinuous acrylamide gradient].

We describe a modified lipoprotein electrophoresis on acrylamide gel. The lipoproteins, prestained with Sudan Black, are separated by running on acrylamide-agarose gels, with two different concentrations of acrylamide and a constant concentration of agarose. The sera are deposited in the first gel (2% acrylamide). Chylomicrons remain at origin and other lipoproteins run through the first gel to the second one (3% acrylamide gel). VLDL stays at the junction of both gels, LDL and HDL are separated in the 3% acrylamide gel. By this technique, we were able to detect an increase of Lp(a) and to identify the different types of hyperlipoproteinemia. After running, the plates can be treated for storage.

Electrophoresis, Agar Gel↗

PubMed1975

Neurotoxicity of acrylamide and its analogues and effects of these analogues and other agents on acrylamide neuropathy.

N-Hydroxymethylacrylamide, N-methylacrylamide, and N,N-diethylacrylamide produce peripheral neuropathy in rats. Seven other compounds related to acrylamide do not produce neuropathy. Rats given one of the three neurotoxic compounds are more susceptible to acrylamide. A regime for testing acrylamide analogues for neuro-toxicity is suggested. DDT, phenobarbitone, or high dietary concentrations of vitamin A or E have no effect on the development of acrylamide neuropathy in rats. Acrylamide produces neuropathy in hens but not in frogs or goldfish.

Acrylamides↗

PubMed1975

Nervous system degeneration produced by acrylamide monomer.

Acrylamide, widely employed as a vinyl monomer in the polymer industry, is a potent neurotoxin to man and to animals. The cumulative effect of prolonged, low-level exposure to acrylamide monomer is the insidious development of a progressive peripheral neuropathy. Sensory symptoms begin in the hands and feet (numbness, pins and needles), certain reflexes are lost and, with severe exposure, muscle weakness and atrophy occur in the extremities. The peripheral neuropathy may be supplemented by symptoms indicative of central nervous system damage (ataxia, tremor, somnolence and mental changes). The neuropathologic basis for this clinical picture has been determined in cats. Here, chronic acrylamide intoxication produces selective peripheral and central nerve fiber degeneration. Degeneration first occurs in the extremities of long and large nerve fibers which later undergo a progressive, seriate proximal axonal degeneration known as dying-back. Especially vulnerable are sensory axons supplying Pacinian corpuscles and muscle spindles in the hindfoot toepads, while adjacent motor nerve axons die back later. Distal central nerve fiber degeneration is seen in the medulla and the cerebellum. The neurotoxic property of acrylamide is of practical concern in two areas. One major problem is the protection of factory workers engaged in the manufacture of acrylamide. A sensitive test of neurologic function in these individuals, i.e., touch sensation, based on the experimental observation of the exquisite vulnerability of Pacinian corpuscles in acrylamide intoxicated cats, is presently under consideration. The second area for concern is the exposure of the populace to minute amounts of neurotoxic acrylamide monomer which contaminate acrylamide polymers currently deployed in the environment. Federal restrictions on the maximum permitted exposure to acrylamide, based on a largely clinical study of acrylamide neurotoxicity conducted ten years ago, may require a re-evaluation in the light of recent advances which have pinpointed the initial sites of nerve fiber degeneration.

Acrylamides↗

PubMed2026

Diving Deeper Into Mechanisms of Acrylamide-Induced Toxicity: RNA Sequencing Reveals Transcriptomic Alteration and Retrotransposon Expression in Drosophila melanogaster.

Given the inevitability of human and animal exposure to acrylamide, there is increasing concern regarding its potential health risks. While a number of molecular mechanisms have been proposed, the complexity of acrylamide toxicological pathways and interactions remains incompletely characterized. In this study, we employed a transcriptomic approach to investigate the transcriptional responses of Drosophila melanogaster following exposure to acrylamide (100 mg/kg). Our analysis identified 634 differentially expressed genes (DEGs), with 362 upregulated and 272 downregulated. Functional analysis revealed these DEGs are enriched in pathways related to reproduction, detoxification, cellular and metabolic processes, signaling, synaptic formation and organization. Notably, acrylamide exposure upregulated the expression of tau and beta-amyloid protein precursor-like genes, both implicated in Alzheimer's disease pathology. An aversive memory test further demonstrated that acrylamide impaired the short-term memory of treated flies. Additionally, acrylamide-induced toxicity altered the expression of nine long terminal repeat retrotransposons, belonging to the gypsy and pao superfamilies. By exploring the potential role of transposable element activity in acrylamide-mediated toxicity, this study provides novel insights into the molecular mechanisms underlying its effects. Collectively, these findings offer a more comprehensive understanding of the mechanisms and pathways associated with the toxic action and detoxification of acrylamide in D. melanogaster.

Animals↗

PubMed1978

The effect of acrylamide on human polymorphonuclear neutrophils in vitro.

Acrylamide (CH2CHCONH2), the vinyl monomer of the industrially useful polymer polyacrylamide, is a recognised neurotoxin. Investigation in our laboratory indicated that, in addition to its neurotoxic effect, acrylamide depressed human polymorphonuclear leucocyte (PMN) chemotaxis in vitro. As genetic or chemical inhibition of PMN phagocytic function frequently pre-disposes patients to repeated bacterila infections, the in vitro effects of acrylamide on several other human PMN functions were studied. Acrylamide in concentrations up to 37.5 mg/ml had no effect on trypan blue uptake. However, bacterial ingestion, killing, and induced chemiluminescence were depressed by pre-treatment with acrylamide (10 mg/ml). It seems unlikely that acrylamide exposure alters host resistance to bacterial infections, because (a) large doses of acrylamide are necessary to interfere with phagocytic functions, (b) acrylamide reacts readily with proteins on many tissue cells and may be made inaccessible or non-toxic to PMN'S and (C) PMNs have a rapid turnover rate in the body and non-functional cells would be rapidly replaced by functional cells.

Acrylamides↗

PubMed2026

Changes in the chick liver structure and blood plasma biochemical properties following in ovo administration of acrylamide.

This study analyzed the effects of acrylamide administration during the embryonic period on liver microstructure and blood plasma biochemical parameters in hatched chicks. On day 6 of incubation, 96 embryonated eggs per group were injected with acrylamide (ACR) at doses of 0.0, 0.25, 0.5, 1.0, 2.0 and 4.0 mg ACR/egg dissolved in 0.9% saline solution (100 µL). Embryo development, hatchability and quality of chicks were evaluated. The ten chicks per group (0.0, 0.25, 0.5 and 1.0 mg ACR/egg) were euthanized immediately after hatching, and blood and liver samples were collected for further analysis. Hatchability was 74.0, 67.7, 66.7 and 49.5% in groups treated with 0.0, 0.25, 0.5, 1.0 mg ACR/egg, respectively, while all embryos died in 2.0 and 4.0 mg ACR/egg groups. Acrylamide intoxication affected only a few biochemical parameters of blood, including a significant decrease in glucose and globulin levels in the group injected with a dose of 1 mg/egg and a significant increase in blood urea nitrogen concentration in the group treated with a dose of 0.5 mg/egg. However, this substance caused negative changes in the microarchitecture of the liver of one-day-old chicks, as indicated by the results of histomorphometric analysis, such as an increase in total hepatocyte nuclei, binucleated hepatocytes, cell nucleus size, collagen area, and other cells. Furthermore, abnormalities in liver structure were confirmed by trace elements content results. Thus, in individuals treated with acrylamide (0.25 and 0.5 mg/egg), a decrease in copper levels and (0.25 mg/egg) nickel and iron levels and an increase in cadmium levels were observed. An increase in lead content was similarly observed in the group exposed to acrylamide at a dose of 0.5 mg/egg, as well as an increase in zinc levels in groups administered various doses of this toxic substance. Overall, the results suggest an inconsistent and dose-dependent toxic effect of acrylamide on liver structure and selected blood plasma parameters in one-day-old chicks.

Acrylamide↗

PubMed1977

[Determination of a small amount of acrylamide in air (author's transl)].

According to the recently published "Guidebook of Measuring Method for Environmental Atmosphere" edited by the Department of Safety and Health Labour Administration of Japan, it is recommended to determine acrylamide (AAM) in air by sampling with glass fiber filter, extracting into methanol and injecting in the FID gaschromatograph (GC). Although acrylamide particle may be measured by this method, it is questionable whether a small amount of gaseous acrylamide could be determined together. We have investigated the determination of a small amount of acrylamide monomer in air by sampling it on solid adsorbent packed in a specially designed sampling tube. We concluded that it is capable to determine a small amount of acrylamide in air, by using the above mentioned sampling tube packed with Flusin-F (treated with phosphoric acid; 30--60 mesh) as the solid adsorbent, at the concentration range from 1.0 to 0.01 ppm (v/v), and the recovery rate of 82--83%.

Acrylamides↗

PubMed1978

Attenuated dynamic responses of primary endings of muscle spindles: a basis for depressed tendon responses in acrylamide neuropathy.

Depressed or lost tendon reflexes commonly observed in patients with peripheral neuropathies may result partly from attenuation of the dynamic discharge from the primary endings of muscle spindles. This possibility was investigated in cats with an experimental neuropathy induced with acrylamide (30 mg/kg/day intramuscularly). Achilles tendon reflexes and the dynamic discharge from primary muscle spindles were evaluated after five or ten injections of acrylamide. After five injections the animals were moderately impaired neurologically, the Achilles tendon reflex was difficult to elicit in 2 of 5 animals, and the dynamic responses of primary endings of soleus muscle spindles to stretch were depressed. Following ten injections of acrylamide the cats were severely impaired neurologically; tendon responses were either absent or difficult to elicit, and the dynamic responses of their muscle spindles to stretch were reduced by 50% (p less than 0.01). Additionally, the spindels responded to stretch with only 20 to 30% the normal number of afferent impulses. These data suggest that lost tendon responses in acrylamide neuropathy result in part from inadequate activation of motoneurons by spindle afferent discharge.

Acrylamides↗

PubMed1978

Inhibition of fast axoplasmic transport by acrylamide.

The effect of acrylamide on fast axoplasmic transport in the cat sciatic nerve was studied in vivo and in vitro by the technique of isotope injection. [14C]leucine was injected into the lumbar dorsal root ganglia. In cats fed daily doses of acrylamide over 1 to 4 weeks, the rate of transport was 286 mm/day compared with 424 mm/day in controls. In vitro incubation of the sciatic nerve with acrylamide (2 x 10(-2) M and 2 x 10(-4) M) demonstrated no such inhibition. Study of the results and review of the literature suggest that acrylamide acted subacutely on metabolism of amino acid and protein in the nerve axon, probably in the smooth endoplasmic reticulum.

Acrylamides↗

PubMed1978

Chromosome aberrations induced by monomeric acrylamide in bone marrow and germ cells of mice.

Acrylamide induces chromatid exchanges and breaks with considerable frequency in spermatogonia of mice with long-term administration (3 weeks), though not, remarkably, with short-term administration (1--2 weeks. At 12 and 24 h after single injections with 50, 100 and 150 mg/kg acrylamide, evaluation of the cytogenetic effect is difficult in the spermatogonia because of an extreme reduction of mitotic cells. Aneuploid and polyploid cells increase with time after treatment in both marrow and spermatogonial cells, while the aberration frequency shows no increase in marrow after both oral-administration and injection. Evidently the spermatogonia are thus rather more sensitive to acrylamide than marrow cells. On the other hand, the SCE frequency is at the control level in treated subjects in marrow and spermatogonia. Acrylamide induces chain quadrivalents, ring quadrivalents, fragments and univalents which are particularly evident in primary spermatocytes in both oral administration and injection, though it is questionable whether these structural changes deal with spermatogonia, or otherwise with the S-phase primary spermatocytes. There is a possibility that the aberrant cells thus produced can develop into spermatozoa carrying a certain type of reciprocal translocation which leads to semi-sterile progeny. In relation to the above problem detailed investigations into this type of rearrangement in primary spermatocytes are needed.

Acrylamides↗

PubMed1978

Position sensitivity of de-efferented muscle spindles in experimental acrylamide neuropathy.

An experimental neuropathy was induced in cats by injections of acrylamide (7.5, 15 or 30 mg/kg/day) for 2 to 10 days. The responses of primary and secondary endings of soleus muscle spindles to stretch were evaluated and correlated with the appearance of ataxia and incoordinated motor movements. Animals that received 15 or 30 mg/kg/day became ataxic and demonstrated poor motor coordination on the 7th or 4th day, respectively. At these times, both primary and secondary endings of muscle spindles had elevated thresholds and diminished discharge frequencies. Continued acrylamide administration resulted in exacerbation of the clinical symptoms and further attenuation of spindle responses. The discontinuation of acrylamide was followed by slow recovery. Only those cats which received a total dose of 75 mg/kg or less remained asymptomatic and had normal spindle function. The coincidence of onset of motor coordination deficits and spindle dysfunction, coupled with a lack of demonstrable motor defect at the same time, suggests that the initial clinical features of acrylamide neuropathy may be partly the consequence of impaired spindle function.

Acrylamides↗

PubMedDate not supplied

Polyneuropathies and CNS protein metabolism. III. Changes in protein synthesis rate induced by acrylamide intoxication.

A defect in neuronal protein metabolism has been proposed as one of the primary, molecular events underlying the development of polyneuropathies of the dying back type. Using acrylamide-intoxication as an experimental model to study these polyneuropathies, changes in leucine-incorporation into proteins disability. Proteinsynthesis rates were determined in vivo using flooding concentrations of [1-14C]valine as the precusor. Under conditions of acute and of chronic intoxication, a decrease in synthesis rate was measured preceding the loss of functional ability. Similar changes in protein synthesis rate were observed in peripheral tissues such as heart muscle and liver showing the general toxicity of acrylamide. Methylene bisacrylamide, that was used to discriminate between the neurotoxic action of acrylamide and its systemic effects, interfered with protein synthesis rates in a comparable way. No change in protein synthesis rate was observed under in vitro conditions suggesting that the interference of acrylamide with the synthetic machinery for protein synthesis in vivo is mediated by one or more as yet unknown indirect factors.

Acrylamides↗

PubMed2026

Furanic compounds in different coffee extraction systems: Analysis of the main influencing factors and correlation with acrylamide.

This study investigates how different coffee types representative of distinct roast profiles and brewing methods jointly affect the occurrence of furanic compounds and acrylamide in brewed coffee. Coffees were prepared using eight extraction methods (AeroPress, Clever, Chemex, French Press, Moka, Pure Brew, Turkish and V60). Five furanic compounds (furfural, furfuryl acetate, 5-methylfurfural, furfuryl alcohol and 5-hydroxymethylfurfural) were quantified in coffee powders and brews by HS-SPME-GC-MS, while acrylamide was determined by UHPLC-MS/MS. Moka and Turkish brews consistently exhibited the highest concentrations of furanic compounds, whereas paper-filtered pour-over methods (V60 and Chemex) showed the lowest levels. Pearson correlation analysis revealed coffee-dependent relationships between furanic compounds, acrylamide and extraction parameters with the strongest associations observed in dark-roasted coffee, reflecting advanced Maillard reaction chemistry. Overall, these results demonstrate that contaminant levels arise from the combined effects of intrinsic coffee chemistry and brewing mechanics and support targeted mitigation strategies: such as roast selection and brewing method optimization.

Acrylamide↗

PubMed2026

Advanced mitigation strategies for acrylamide formation in foods: Mechanistic insights, emerging innovations, and future perspectives.

Acrylamide is a heat-induced contaminant formed predominantly in carbohydrate-rich foods during high-temperature processing, posing significant concerns due to its potential carcinogenic, neurotoxic, and genotoxic effects. This review critically examines the mechanisms of acrylamide formation, emphasizing the role of the Maillard reaction and key precursors such as asparagine and reducing sugars, along with the influence of processing conditions including temperature, time, pH, and moisture. Various mitigation strategies are comprehensively discussed, ranging from raw material selection and genetic approaches to enzymatic treatments such as asparaginase and the application of natural and chemical inhibitors. Advances in processing technologies, including optimization of conventional thermal methods and emerging non-thermal techniques such as cold plasma and ultrasound, are evaluated for their effectiveness. The review also highlights the role of food additives, functional ingredients, and fermentation in reducing acrylamide formation. Furthermore, recent developments in analytical techniques, including chromatographic methods, biosensors, and artificial intelligence-based predictive models, are explored for improved detection and control. Risk assessment, toxicological implications, and global regulatory frameworks are also examined. Finally, future perspectives focusing on genetic engineering, personalized nutrition, and digital technologies such as AI and blockchain are discussed to support sustainable and industry-applicable mitigation strategies.

Acrylamide↗

PubMed1975

Physiological studies of the dying-back phenomenon. Muscle stretch afferents in acrylamide neuropathy.

(1) The responses of 1,001 medial gastrocnemius afferents with conduction velocities of 24-126 m/sec have been studied in cats with experimental acrylamide neuropathy. (2) Many units which conducted at velocities indicating that they innervated muscle stretch receptors failed to discharge during muscle stretch or contraction. In animals with mild neuropathy 10 per cent of 366 units were non-responsive. In animals with moderate or severe neuropathy the proportion of non-responsive units was 68 per cent of 315 fibres and 89 per cent of 320 fibres respectively. Group I fibres were involved to a greater extent than Group II fibres. (3) The distributions of identified functioning units with respect to conduction velocity were normal, indicating that acrylamide did not produce conduction slowing before failure of function. (4) Electrophysiological and histological findings indicate that acrylamide initially produces failure of impluse conduction and subsequent fibre breakdown in the terminal axon while normal impulse conduction is preserved more proximally.

Acrylamides↗

PubMed1978

Electrophoretic characterization of the nonspecific esterases of the mosquito, Culex tarsalis: conventional and isoelectric focused acrylamide gels.

1. The nonspecific esterases of the mosquito, Culex tarsalis, were examined through conventional and isoelectric focusing acrylamide gel electrophoresis. 2. Conventional acrylamide gel electrophoresis resolved five components. These were characterized as: three carboxylesterases, one acetylcholinesterase and one acetylesterase. 3. Isoelectric focusing resolved 18 components. These were characterized as: 14 carboxylesterases, two acetylcholinesterases, one acetylesterase and one arylesterase. 4. The reproducibility and reliability of isoelectric focusing is discussed and compared to conventional acrylamide gel electrophoresis for the examination of multi-component isozyme systems such as non-specific esterases.

Animals↗

PubMed1975

Oxygen consumption by acrylamide polymerization: a method for rapid screening of anticancer agents.

We have developed a rapid and sensitive method to measure oxygen consumption of tumor cells by acrylamide polymerization. This method could be used as an in vitro screen for potential chemotherapeutic agents. Previous techniques have lacked either the sensitivity or the speed required for use as an effective clinical tool. This method was modified from a technique previously developed in our laboratory for measuring oxygen in blood. Standard anticancer agents were tested against Walker 256 ascites tumor. Ascites was harvested from 20 rats on each of 50 days, incubated briefly with drugs, and acrylamide polymerization time was measured hourly. Individual controls were established for each drug-treated group, and oxygen uptake measured after one hour of incubation. Actinomycin, cyclohexamide, and cytosine arabinoside inhibited tumor cell oxygen consumption by 80%, 40%, and 30%, respectively. These results correlated with the known in vivo effects of these drugs on Walker carcinosarcoma. Therefore, this sensitive method could potentially be used directly on tumor cells removed from biopsy material so that the testing of anticancer drugs could be completed on the day of biopsy.

Acrylamides↗

PubMed1978

Unmyelinated nerve fibres in feline acrylamide neuropathy.

Electronmicroscope studies have been performed on the greater splanchnic nerve and the nerve to the medial head of gastrocnemius muscle of control and acrylamide poisoned cats. Degeneration of unmyelinated as well as of myelinated fibres was observed in both nerves. In cats severely poisoned with acrylamide, some very large unmyelinated axons undergoing early degeneration were seen in the splanchnic nerve. In the nerve to medial head of gastrocnemius, there was a decrease in the proportion of large diameter unmyelinated axons.

Acrylamides↗