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PubMed2005

Acrylamide-occurrence in mixed concentrate feed for dairy cows and carry-over into milk.

During the preparation of cooked foods acrylamide is formed from asparagine and reducing sugars at high temperatures. By-products of oil, starch and sugar production, which may be found in animal feed, partially result from processing steps using heat treatment that are similarly likely to form acrylamide. Possibly, pelletizing during the processing of mixed concentrates may also be involved in acrylamide formation. Thus the occurrence of acrylamide in animal feed and the potential for carry-over into animal products should be tested. Independently of the feed matrix, 1.5 g per day of acrylamide was fed to a cow for ten days resulting in a mean concentration of 175 microg/kg of acrylamide in the milk. From the data obtained the mean carry-over was found to be 0.24%, and a mean half-life time of 2.8 h was estimated. This means acrylamide was rapidly transformed in the cow. The acrylamide concentrations in three commercial mixed concentrates were respectively 180, 145 and 140 microg/kg feed. To test the possible effect of pelletizing, the peripheral zones were separately analysed. No difference in concentration was observed. Based on the carry-over rate estimated in this study, a maximum concentration of approx. 0.2 microg/kg of acrylamide would be expected in milk from cows fed with such feeds.

Acrylamide↗

PubMed2001

The multiplicative model for cancer risk assessment: applicability to acrylamide.

According to a multiplicative model for prediction of cancer risk for genotoxic agents the incremental cancer risk is, for low-intermediate exposures, proportional to target doses of the genotoxic substance and to the background risk in control groups. This model has been applied to evaluate cancer tests of acrylamide in rodents. Because of its reactivity toward DNA, glycidamide is assumed to be the causative genotoxic metabolite of acrylamide. Evaluation of experimental data according to the multiplicative model shows that mice, compared with rats, are of the order of 10 times more sensitive per administered dose of acrylamide. The US EPA procedure would, however, generally predict rats to be about twice as sensitive as mice to carcinogenic chemicals, because their estimates are based on scaling of the dose per square meter body surface area, as a surrogate for metabolic differences between the species. The comparison of rats and mice with respect to observed cancer incidence is at a key position in the evaluation of the usefulness of risk models for extrapolation between species. In the present study mice and rats were compared, with respect to in vivo doses of acrylamide and the metabolite glycidamide, after exposure to acrylamide. The relative in vivo doses were inferred from levels of hemoglobin adducts. The adduct levels from glycidamide were, per administered dose of acrylamide, approximately 3-10 times higher in mice than in rats. In combination with the above mentioned higher sensitivity of mice than rats in cancer tests of acrylamide this is compatible with the concept that glycidamide is the key genotoxic factor in acrylamide exposure. Furthermore, it is shown that the multiplicative, i.e. relative, risk model and measurements of the dose of the genotoxic factor give good prediction of the observed risk from acrylamide in cancer tests with rats and mice.

Acrylamide↗

PubMed2004

Genotoxicity of acrylamide and glycidamide.

BACKGROUND: Acrylamide, a known rodent carcinogen, is found in the human diet. However, the mechanism by which acrylamide exerts its carcinogenic effects remains unclear. METHODS: Normal human bronchial epithelial cells and Big Blue mouse embryonic fibroblasts that carry a lambda phage cII transgene were treated in vitro with acrylamide, its primary epoxide metabolite glycidamide, or water (control) and then subjected to terminal transferase-dependent polymerase chain reaction to map the formation of DNA adducts within the human gene encoding p53 (TP53) and the cII transgene. The frequency and spectrum of glycidamide-induced mutations in cII were examined by using a lambda phage-based mutation detection system and DNA sequence analysis, respectively. All statistical tests were two-sided. RESULTS: Acrylamide and glycidamide formed DNA adducts at similar specific locations within TP53 and cII, and DNA adduct formation was more pronounced after glycidamide treatment than after acrylamide treatment at all doses tested. Acrylamide-DNA adduct formation was saturable, whereas the formation of most glycidamide-DNA adducts was dose-dependent. Glycidamide treatment dose-dependently increased the frequency of cII mutations relative to control treatment (P<.001). Glycidamide was more mutagenic than acrylamide at any given dose. The spectrum of glycidamide-induced cII mutations was statistically significantly different from the spectrum of spontaneously occurring mutations in the control-treated cells (P=.038). Compared with spontaneous mutations in control cells, cells treated with glycidamide or acrylamide had more A-->G transitions and G-->C transversions and glycidamide-treated cells had more G-->T transversions (P<.001). CONCLUSION: The mutagenicity of acrylamide in human and mouse cells is based on the capacity of its epoxide metabolite glycidamide to form DNA adducts.

Acrylamide↗

PubMed2005

Effects of acrylamide on primary neonatal rat astrocyte functions.

The present study assessed biochemical endpoints indicative of acrylamide toxicity in astrocyte cultures derived from neonatal rat pups. Given earlier reports on the possible ability of acrylamide to induce astrocytomas in the Fischer 344 rat, we performed studies in neonatal rat astrocyte cultures from the Fischer 344 to assess the ability of acrylamide to induce astrocytic proliferation. Measurements on astrocytic proliferation included [3H]-leucine incorporation, [3H]-thymidine incorporation, and changes in proliferating cell nuclear antigen (PCNA). Although acrylamide (0.1 and 1 mM for 7, 11, 15, or 20 days) did not significantly (P > 0.05) affect [3H]-leucine or [3H]-thymidine incorporation, it significantly (P < 0.05) increased PCNA protein expression in astrocytes exposed to acrylamide for 15 and 20 days. Additional studies revealed that this effect on PCNA protein expression was not associated with activation of dopamine-2 (D2) receptors, given that quinpirole (10 microM added to cultures for the last hour of 7, 11, 15, or 20 days in culture), a selective D2 receptor agonist, did not produce results analogous to those seen with acrylamide treatment. Cotreatment of astrocytes with acrylamide (7, 11, 15, or 20 days) and the D2 receptor antagonist, sulpiride (1 microM for the last 6 h of exposure), also failed to reverse acrylamide's effect on PCNA protein induction. Taken together, these studies suggest that acrylamide promotes astrocytic cell proliferation in the CNS even though DNA synthesis did not appear stimulated.

Acrylamide↗

PubMed1999

Mortality patterns among workers exposed to acrylamide: 1994 follow up.

OBJECTIVE: To update the mortality experience of a cohort of 8508 workers with potential exposure to acrylamide at three plants in the United States from 1984-94. METHODS: Analyses of standardised mortality ratios (SMR) with national and local rates and relative risk (RR) regression modelling were performed to assess site specific cancer risks by demographic and work history factors, and exposure indicators for acrylamide and muriatic acid. RESULTS: For the 1925-94 study period, excess and deficit overall mortality risks were found for cancer sites of interest: brain and other central nervous system (CNS) (SMR 0.65, 95% confidence interval (95% CI) 0.36 to 1.09), thyroid gland (SMR 2.11, 95% CI 0.44 to 6.17), testis and other male genital organs (SMR 0.28, 95% CI 0.01 to 1.59), and cancer of the respiratory system (SMR 1.10, 95% CI 0.99 to 1.22); however, none was significant or associated with exposure to acrylamide. A previously reported excess mortality risk of cancer of the respiratory system at one plant remained increased among workers with potential exposure to muriatic acid (RR 1.50, 95% CI 0.86 to 2.59), but was only slightly increased among workers exposed or unexposed to acrylamide. In an exploratory exposure-response analysis of rectal, oesophageal, pancreatic, and kidney cancer, we found increased SMRs for some categories of exposure to acrylamide, but little evidence of an exposure-response relation. A significant 2.26-fold risk (95% CI 1.03 to 4.29) was found for pancreatic cancer among workers with cumulative exposure to acrylamide > 0.30 mg/m3.years; however, no consistent exposure-response relations were detected with the exposure measures considered when RR regression models were adjusted for time since first exposure to acrylamide. CONCLUSION: The contribution of 1115 additional deaths and nearly 60,000 person-years over the 11 year follow up period corroborate the original cohort study findings of little evidence for a causal relation between exposure to acrylamide and mortality from any cancer sites, including those of initial interest. This is the most definitive study of the human carcinogenic potential of exposure to acrylamide conducted to date.

Acrylamide↗

PubMed2005

Current status of acrylamide research in food: measurement, safety assessment, and formation.

Relatively high amounts of acrylamide have recently been reported in carbohydrate-rich foods under low moisture conditions. This sparked intensive investigations into acrylamide, encompassing its occurrence, chemistry, and toxicology/potential health risk in the human diet. Robust and efficient analytical methods have been developed to obtain reliable quantitative data. Recent epidemiological studies failed to evidence an association of cancer incidence and dietary acrylamide exposure. The link of acrylamide in foods to Maillard-type reactions and, in particular, to asparagine has been a major step in elucidating feasible chemical formation routes. Decarboxylation of the Schiff base derived from asparagine and a carbonyl reactant plays a key role in acrylamide formation leading to azomethine ylide intermediates, which offer an attractive mechanistic explanation of the acrylamide amounts found experimentally, including the fact that acrylamide is preferentially formed in the presence of fructose, as compared to glucose or alpha-dicarbonyls. However, the physical state of the reaction system may also affect acrylamide formation by influencing molecular mobility, particularly under low moisture conditions. Current research deals mainly with mitigation studies to reduce acrylamide during food processing and the role of water.

Acrylamide↗

PubMedDate not supplied

Acrylamide and polyacrylamide: a review of production, use, environmental fate and neurotoxicity.

Acrylamide is a highly water soluble vinyl monomer formed from the hydration of acrylonitrile. The major commercial use of acrylamide is the formation of polymers. In the environment acrylamide has a high mobility in soil, may travel great distances in ground-water, is biodegradable, and is not absorbed by sediments or affected by water treatment. It is absorbed by all routes of animal exposure. The main metabolite is N-acetyl-S-(3-amino-3-oxypropyl)-cysteine and is excreted predominantly in the urine. Acrylamide produces an ascending central/peripheral axonopathy in man and animals. The major histological findings are swelling of axons and/or decrease in number of large diameter axons. Acrylamide axonopathy is reversible with time, but full recovery depends upon the severity of the intoxication. All reported cases of acrylamide toxicity have been attributed to handling the monomer. Polyacrylamide is non-toxic. Specific clinical features of acrylamide intoxication are more conclusive than electrophysiological, histological or biochemical laboratory tests for diagnosis. Acrylamide can be detected by titration, colorimetry, high performance chromatography, gas chromatography and polarography in air, water, biological fluids, tissues and polyacrylamides. Present research on the effects of acrylamide focuses on developmental and reproductive effects, genotoxicity and carcinogenicity.

Acrylamides↗

PubMed2002

[Study on production of acrylamide by microbial method (II)--enzyme catalytic kinetics and de-active dynamics of nitrile hydratase].

The hydration reaction by microbial method is the crisis of the procedure of acrylamide production from acrylonitrile. This research studied the enzyme catalytic kinetics and de-active kinetics of nitrile hydratase in the type of free cell. Firstly, the effects of the concentration of cells, the temperature, pH value, the concentration of acrylonitrile and the concentration of acrylamide on the activity of nitrile hydratase was investigated. The result is that the temperature and the concentration of acrylamide are the most important among these factors. The activity of the nitrile hydratase was 5659 u/mL (broth) at 28 degrees C; the counterpart was only 663 u/mL (broth) at 5 degrees C. And the activity of NHase in solution of 45% acrylamide was just about half of that in solution of 5% acrylamide. After study on the relation of temperature and the reaction speed, It was found that the activation energy of the hydration of NHase was 65.57 kJ.mol-1. This paper studied the effects of concentration of cells, temperature, pH value, concentrations of acrylonitrile and acrylamide on the deactivation of Nhase, as well as the related enzyme de-active kinetics. The result also showed that the temperature and the concentration of acrylamide are the most important among these factors. In solution of 35% acrylamide, the residual activity was about 0% of the original value after 55 h; but in solution of 10% acrylamide, after the same period of time, the residual activity was 50% of the original one. It was also found that the concentration of acrylonitrile had little effect on the stability of NHase. The coefficient of deactivation at 28 degrees C was 21.77 times of the one at 5 degrees C. Correlating the temperature and the coefficient of deactivation, the activation energy of the de-active reaction was found to be 92.28 kJ.mol-1.

Acrylamide↗

PubMed2005

[Determination of acrylamide in fried starchy foods by gas chromatography-mass spectrometry].

A method was developed for the determination of acrylamide in fried starchy foods using isotope dilution gas chromatograpy-selected mass spectrometry (GC-MS). The acrylamide was extracted from samples by water, then centrifuged and cleaned up by a column of graphitized carbon black. Acrylamide was derivatized through bromination at low pH and low temperature and determined by GC-MS. With the aid of the 13C-substituted acrylamide internal standard, the mass spectrum in GC-MS was interpreted, and the content of acrylamide was measured. The limit of quantitative detection (S/N > 10) was 5 microg/kg and the recovery was in the range of 90%-105% and relative standard deviation is 6.3%. The levels of acrylamide in some fried foodstuffs such as French fries was surveyed using the method. French fries were found to contain 278-4518 microg/kg acrylamide. It means that the content of acrylamide in French fries is 10,000 times higher than the drinking water guideline of World Health Organization for acrylamide.

Acrylamide↗

PubMed1985

Inhibition of glyceraldehyde-3-phosphate dehydrogenase in tissues of the rat by acrylamide and related compounds.

In previous investigations acrylamide was found to inhibit several enzymes of glycolysis both in vitro and in vivo. The present study examines the characteristics of the in vitro inhibition of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and compares the in vivo effects of acrylamide on GAPDH activity to other analogs. Inhibition of GAPDH produced by acrylamide was characteristic of an irreversible or slowly reversible mechanism. In vivo, GAPDH activity was determined in sciatic nerve, brain, skeletal muscle and liver after cumulative doses of 250, 350 or 500 mg/kg of acrylamide. Specific activities were significantly lower in extensor muscle and liver after the 250 mg/kg dose. Activities in brain and sciatic nerve tended to be decreased but the differences were not statistically significant. Specific activity of GAPDH was decreased in medulla pons, cerebellum and the rest of the brain after a 350 mg/kg cumulative dose of acrylamide, although protein concentrations were not different from those in controls. The maximum decrease was about 20%. Treatment with acrylamide, methylene-bis-acrylamide (non-neurotoxic), or N-isopropylacrylamide (neurotoxic) significantly decreased the weight of the cortex and associated brain areas as well as general body weights. No signs of developing neuropathy were observed during treatment with methylene-bis-acrylamide to a cumulative dose (8.1 mmoles/kg) equivalent to that of acrylamide causing frank paralysis. Although the compound exhibited some ability to inhibit GAPDH in vitro, no decrease in GAPDH activity was found in rat brain. Treatment with N-isopropylacrylamide resulted in progressive neurologic impairment. After treatment to a cumulative dose of the compound causing a severe hind-limb paralysis (9.2 mmoles/kg), a small but significant decrease in GAPDH was found in the three areas of brain examined.

Acrylamides↗

PubMed1981

Antagonism of acrylamide neurotoxicity by supplementation with vitamin B6.

The effect of vitamin B6 supplementation on acrylamide induced neurotoxicity was examined in rats chronically dosed for 3 weeks. Using the inclined screen test, the onset of neurotoxicity developed on day 12 in all rats given 30 mg/kg acrylamide per day on day 16 in the rats supplemented with 5 mg/day of vitamin B6. On day 21 all animals given only acrylamide were severely affected compared to only 4 of 7 rats receiving acrylamide + vitamin B6. Another behavioral index, the foot spread test, did not detect any alteration in the development of acrylamide toxicity by vitamin B6. Weight loss was seen in both acrylamide treated groups and was not altered by vitamin B6 supplementation. The data show that vitamin B6 supplementation can delay the onset and reduce the severity of the neurotoxicity caused by chronic acrylamide administration to rats and suggest that acrylamide toxicity may be caused by an interaction of acrylamide with enzymes involved in supplying energy to the neuron. Vitamin B6 supplementation may be able to increase the amount of energy available to the neuron via alternate metabolic pathways.

Acrylamides↗

PubMed1990

Cytoskeletal dynamics in rabbit synovial fibroblasts: I. Effects of acrylamide on intermediate filaments and microfilaments.

Rabbit synovial fibroblasts respond to changes in cell shape and cytoskeletal architecture by altering specific gene expression. We have tested the ability of acrylamide, a neurotoxin that alters the distribution of intermediate filaments in cultured PtK1 cells, to induce metalloprotease expression in synovial fibroblasts. Cells treated with 2-20 mM acrylamide for 5 to 24 h underwent shape changes similar to cells treated with the tumor promoter phorbol myristate acetate. Intermediate filaments visualized with anti-vimentin antibodies did not collapse into a perinuclear cap in these rounded cells, but were still present in the extended cell processes. Unexpectedly, when actin was visualized in acrylamide-treated cells, extensive dissociation and clumping of microfilaments was observed. Concentrations of acrylamide greater than 10 mM were cytotoxic, but cells recovered completely after 24 h incubation with 5 mM acrylamide. Like other agents that alter cell shape and actin distribution in synovial fibroblasts, acrylamide also induced expression of the secreted metalloprotease collagenase. Although some recent evidence suggests that acrylamide may be able to exert its collagenase-inducing effects extracellularly, perhaps through transmembrane matrix receptors, our observation that this neurotoxin dramatically alters protein synthesis in synovial fibroblasts suggests that direct effects on cell metabolism may also play a role in acute acrylamide intoxication.

Acrylamide↗

PubMed1986

The effect of acrylamide on hepatocellular DNA repair.

Acrylamide has recently been reported to induce tumors in laboratory animals. The effect of acrylamide on unscheduled DNA synthesis using the hepatocyte primary culture (HPC)/DNA repair test was examined. Isolated hepatocytes were exposed to acrylamide and [3H]thymidine ( [3H]TdR) for 18 hr. Incorporation of [3H]TdR into DNA was determined by autoradiography. No DNA repair was observed at acrylamide concentrations up to 10(-2) M. These findings were confirmed using density gradients. Acrylamide concentrations exceeding 10(-2) M were cytotoxic to hepatocytes. Because both autoradiography and density gradients measure DNA repair as an endpoint, the ability of acrylamide to inhibit these repair processes was also determined. Acrylamide had no effect on the repair of UV-damaged DNA. These results show that acrylamide is not genotoxic in isolated hepatocytes.

Acrylamide↗

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↗

PubMed1994

Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide.

A study was performed among 41 workers heavily exposed to a mixture of acrylamide and acrylonitrile in the city of Xinxiang, Henan province, People's Republic of China. The workers underwent a complete medical and neurological examination and provided blood and urine for the determination of several biomarkers of exposure. Among the exposed workers, signs and symptoms indicating peripheral neuropathy were found with statistically significant increased frequencies compared to a group of controls from the same city. Based on neuropathic signs and symptoms and quantifiable indicators of peripheral nervous dysfunction, such as vibration thresholds and electroneuromyography measurements, a neurotoxicity index (NIn) specific for acrylamide-induced peripheral neuropathy was designed. The NIn, which adequately predicted the clinical diagnosis of peripheral neuropathy, was significantly correlated with the levels of mercapturic acids in 24-hr urine, hemoglobin adducts of acrylamide, accumulated in vivo doses of acrylamide, employment time, and vibration sensitivity. The NIn was correlated also with hemoglobin adducts of acrylonitrile, which was explained primarily by a correlation between acrylamide and acrylonitrile exposure in this workshop. However, it was not significantly correlated with momentary measures of exposure such as concentrations of acrylamide in the air or in the plasma of exposed workers. This study is the first in which adduct monitoring has been applied to the same group of individuals in which adverse health effects have been observed. The results seem to indicate that hemoglobin adducts are useful as predictors of acrylamide-induced peripheral neuropathy and that measurements of vibration thresholds are useful for identifying early neurotoxic effects in workplaces with hazardous exposures to acrylamide.

Acetylcysteine↗

PubMed1994

Acrylamide alters neurofilament protein gene expression in rat brain.

Acrylamide, a prototype neurotoxin, alters neurofilament protein (NF) gene expression in rat brain. Levels of mRNA coding for neurofilament protein subunits NF-L, NF-M, and NF-H have been determined by Northern blot analysis using 32P-labeled cDNA probes. Acrylamide given acutely (100 mg/kg, single intraperitoneal injection) causes a selective increase in NF-M mRNA (approximately 50%) compared to controls. The expression of NF-L or NF-H mRNA is not affected by acrylamide. In contrast, chronic treatment with acrylamide [0.03% (w/v) in drinking water for 4 weeks] induces a modest but significant increase (approximately 22%) in NF-L mRNA compared to controls. Levels of NF-M, and NF-H mRNA are not altered by acrylamide treatment. The expression of beta-actin mRNA, an ubiquitous protein, is not affected by either treatment regimen of acrylamide. The results of this study show that acrylamide increases the expression of mRNA for NF protein subunits in rat brain. The increase of specific mRNA for NF subunits depends on the dose, duration and route of acrylamide administration.

Acrylamide↗

PubMed1993

Acrylamide-induced depletion of microtubule-associated proteins (MAP1 and MAP2) in the rat extrapyramidal system.

Acrylamide, an occupational neurotoxicant, reduced MAP1 and MAP2 distribution in different regions of rat brain. Different components of the extrapyramidal system (caudate-putamen, globus pallidus, substantia nigra and red nucleus) revealed differential distribution of MAP1 and MAP2 in acrylamide-treated animals. Rats were treated with acrylamide (estimated mean dose: 15 mg/kg/day) for 2 weeks and MAP1 and MAP2 were localized according to Sternberger's peroxidase-anti-peroxidase technique. MAP1 labelled neuronal perikarya and dendrites almost with a similar intensity, but MAP2 immunostaining was more intense in dendrites than neuronal perikarya. Acrylamide caused a near-total loss of MAP1 and MAP2 immunoreactivity in caudate-putamen. Other components of the extrapyramidal system were relatively less affected by acrylamide. These results indicate that caudate-putamen is more susceptible to the action of acrylamide than other components of the extrapyramidal system studied. The depletion of MAP1 and MAP2 immunoreactivity by acrylamide appears to be an early biochemical event preceding peripheral neuropathy. The loss of MAPs immunoreactivity occurs first in dendrites and proceeds toward the perikarya. This study indicates that acrylamide not only causes axonal damage but may also induce dendritic degeneration.

Acrylamide↗

PubMed1994

Effects of acrylamide on cotransmission in perivascular sympathetic and sensory nerves.

The effects of chronic administration of acrylamide on sympathetic and sensory nerves were examined in the mesenteric artery of rabbits. The noradrenaline (NA) content of the artery was significantly decreased and the total contractile response to electrical field stimulation (4-64 Hz) markedly reduced in the acrylamide group. This was not due to an impairment of the contractility of the smooth muscle or to alterations in the postjunctional receptors. At 16 Hz, only the purinergic component of sympathetic cotransmission was significantly reduced by acrylamide. At 64 Hz, both the purinergic and the adrenergic components were significantly decreased. Field stimulation of the artery pretreated with guanethidine and precontracted with NA produced a frequency-dependent relaxation which was prevented by capsaicin and thus mediated by perivascular sensory nerves. In contrast to its effects on sympathetic cotransmission, acrylamide resulted in a trend, although not significant, towards increased responses at each frequency studied (2-16 Hz). 2-Methylthio-ATP (2Me-S-ATP) caused significantly greater relaxation following acrylamide treatment while vasodilator responses to calcitonin gene-related peptide and substance P were unchanged. It is concluded that, in addition to its known action in producing neuropathy in myelinated somatic motor and sensory nerves, acrylamide causes damage to unmyelinated perivascular sympathetic fibres. Purinergic mechanisms may be particularly susceptible to acrylamide since both the purinergic component of sympathetic vasoconstriction and the relaxation in response to 2Me-S-ATP were affected by acrylamide treatment.

Acrylamide↗