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PubMed2005

Genotoxicity and toxicological effects of acrylamide on reproductive system in male rats.

The toxicity of acrylamide was evaluated through mutagenicity of Salmonella, chromosome aberration of Chinese hamster lung fibroblasts, micronucleus formation in mice and reproductive toxicity in rats. Based on Ames test, acrylamide showed mutagenic potency for strains TA98 and TA100. Moreover, both chromosomal aberration assay and micronucleus assay indicated that acrylamide might have genotoxic potency; the chromosomal aberration frequencies were observed to be proportional to acrylamide concentrations of 5-50 mM, and acrylamide significantly increased micronuclei in peripheral blood cells of mice at doses of higher than 72.5 mg/kg. Male rats were treated with acrylamide at doses of 0, 5, 15, 30, 45, or 60 mg/kg/day for 5 consecutive days, and the toxicity of acrylamide was observed. In the group treated with the highest dose of acrylamide (60 mg/kg/day), the loss of body weight and reduced testis weight were observed. Also the epididymides weights were reduced significantly in all the groups treated with acrylamide. The number of sperms in cauda epididymidis decreased significantly in an acrylamide dose-dependent manner. Rats treated with 60 mg/kg/day of acrylamide showed several histopathological lesions in the seminiferous tubules. There were thickening and multiple layering of the tubular endothelium, and the formation of many multinucleated giant cells in seminiferous tubules. Taken together, acrylamide not only causes the genotoxicity of eukaryotic cells and mice but also shows the toxicological effects on reproductive system in male rats.

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PubMed2004

Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population.

Acrylamide (AA) is a food-borne toxicant suspected to be carcinogenic to humans. It is formed in the heating process of starch-containing food. Currently, there is a great discussion about the possible human health risks connected with the dietary uptake of acrylamide. Haemoglobin adducts of acrylamide and its oxidative metabolite glycidamide are both markers of biochemical effect. However, because glycidamide has a higher carcinogenic potency than acrylamide itself, the glycidamide adduct might mirror the genotoxicity better than acrylamide adducts. In order to gain more information about the human metabolism of acrylamide, we investigated a small group of persons for the effective internal doses of acrylamide and glycidamide using haemoglobin adducts as parameters of biochemical effect. The collective was subdivided into non-smokers (n=13) and smokers (n=16) by determining the smoking-specific acrylonitrile haemoglobin adduct (N-cyanoethylvaline, CEV). The mean values for the adducts of acrylamide (N-2-carbamoylethylvaline, AAVal) and glycidamide (N-(R,S)-2-hydroxy-2-carbamoylethylvaline, GAVal) in nonsmokers was 19 pmol/g globin AAVal (range 7-31 pmol/g globin) and 17 pmol/g globin GAVal (range 9-23 pmol/g globin). For smokers mean levels of AAVal were 80 pmol/g globin (range: 25-199 pmol/g globin) and those of GAVal were 53 pmol/g globin (range: 22-119 pmol/g globin). Metabolism to glycidamide turned out to be significantly more effective in non-smokers than in the higher exposed smokers. Compared with studies in rats, the metabolic conversion of acrylamide to glycidamide as measured by haemoglobin adducts seems to occur to a similar extent in humans as in rats. Risk estimations on acrylamide based on experimental data obtained in rats obviously did not overestimate the cancer risk for the general population. Furthermore, our results might indicate that the dose-response curve for acrylamide is not linear. This would be in line with the results of animal experiments on rodents.

Acrylamide↗

PubMed1990

The interaction of acrylamide with glyceraldehyde-3-phosphate dehydrogenase. Structural modifications in the enzyme studied by fluorescence techniques.

The interaction of acrylamide with rabbit muscle glyceraldehyde-3-phosphate dehydrogenase (GPDH) has been investigated in Tris buffer, pH 7.5. When GPDH containing about 1 mol NAD per mol of tetramer is incubated with acrylamide (0.01-0.1 M), the tryptophan emission of GPDH, initially quenched by acrylamide, slowly increases to a value exceeding that recorded before the addition of acrylamide. This effect is not observed in apoenzyme solutions, indicating that the enhancement of fluorescence results from the dissociation of some NAD from the acrylamide treated GPDH. Acrylamide inactivates GPDH but 1 mM NAD protects the enzyme from inactivation. The addition of acrylamide to GPDH, labeled with fluorescein-5-isothiocyanate (GPDH-FITC) increases the fluorescence and decreases the polarization of fluorescein. The fluorescent sulfhydryl reagent N-iodoacetyl-N'-(5-sulfo-1-naphthyl)ethylenediamine induces similar changes in the fluorescence properties of GPDH-FITC. This reagent, however, fails to react with GPDH preincubated with acrylamide and the titration of acrylamide treated GPDH with the sulfhydryl reagent 5,5'-dithiobis(2-nitrobenzoic acid) indicates the loss of up to 7 cysteine residues per tetramer. Acrylamide also decreases the heat stability of GPDH. Altogether, the data indicate that acrylamide covalently reacts with the active site cysteine residues of GPDH and subsequently induces a conformational change in the enzyme.

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PubMed2004

Genotoxicity of acrylamide in human lymphocytes.

Acrylamide is used in the industry and can be a by-product in a high-temperature food processing. It is reported to interact with DNA, but the mechanism of this interaction is not fully understood. In the present study, we investigated the DNA-damaging potential of acrylamide (ACM) in normal human lymphocytes using the alkaline-, neutral- and 12.1 versions of the comet assay and pulsed-field gel electrophoresis. We also investigated effect of acrylamide on caspase-3 activity as well as its influence on the repair process of hydrogen peroxide-induced DNA damage. Acrylamide at 0.5-50 microM induced mainly alkali-labile sites. This damage was repaired during a 60-min repair incubation. Post-treatment of the damaged DNA with repair enzymes: thymine glycol DNA N-glycosylase (Nth) and formamidopyrimidine-DNA glycosylase (Fpg), recognizing oxidized DNA bases, as well as 3-methyladenine-DNA glycosylase II (Alk A), recognizing alkylated bases, caused an increase in the extent of DNA damage, indicating the induction of oxidative and alkylative DNA base modifications by acrylamide. Pre-treatment of the lymphocytes with N-tert-butyl-alpha-phenylnitrone (PBN), a spin trap, as well as vitamins C and E decreased the DNA-damaging effect of acrylamide, which suggest that free radicals/reactive oxygen species may be involved in this effect. Acrylamide impaired the repair of DNA damaged by hydrogen peroxide and increased the activity of caspase-3, which may indicate its potential to induce apoptosis. Our results suggest that acrylamide may exert a wide spectrum of diverse effects on DNA of normal cells, including mostly DNA base modifications and apoptosis. Acrylamide may also impair DNA repair. Free radicals may underline these effects and some dietary antioxidants can be considered as protective agents against genotoxic action of acrylamide. As normal lymphocytes contain cyp2e1 and P450, engaged in the bioactivation of ACM to glicidamide it is uncertain whether acrylamide causes all of measured effect per se or this is the result of the action of its metabolites.

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PubMed2005

Absence of acrylamide-induced genotoxicity in CYP2E1-null mice: evidence consistent with a glycidamide-mediated effect.

Acrylamide, an animal carcinogen and germ cell mutagen present at low (ppm) levels in heated carbohydrate-containing foodstuffs, is oxidized by cytochrome P4502E1 (CYP2E1) to the epoxide glycidamide, which is believed to be responsible for the mutagenic and carcinogenic activity of acrylamide. We recently reported a comparison of the effects of acrylamide on the genetic integrity of germ cells of male wild-type and CYP2E1-null mice [B.I. Ghanayem, K.L. Witt, L. El-Hadri, U. Hoffler, G.E. Kissling, M.D. Shelby, J.B. Bishop, Comparison of germ-cell mutagenicity in male CYP2E1-null and wild-type mice treated with acrylamide: evidence supporting a glycidamide-mediated effect, Biol. Reprod. 72 (2005) 157-163]. In those experiments, dose-related increases in dominant lethal mutations were detected in uterine contents of female mice mated to acrylamide-treated wild-type males but not CYP2E1-null males, clearly implicating CYP2E1-mediated formation of glycidamide in the induction of genetic damage in male germ cells. We hypothesized that acrylamide-induced somatic cell damage is also caused by glycidamide. Therefore, to examine this hypothesis, female wild-type and CYP2E1-null mice were administered acrylamide (0, 25, 50mg/kg) by intraperitoneal injection once daily for 5 consecutive days. Twenty-four hours after the final treatment, blood and tissue samples were collected. Erythrocyte micronucleus frequencies were determined using flow cytometry and DNA damage was assessed in leukocytes, liver, and lung using the alkaline (pH>13) single cell gel electrophoresis (Comet) assay. Results were consistent with the earlier observations in male germ cells: significant dose-related increases in micronucleated erythrocytes and DNA damage in somatic cells were induced in acrylamide-treated wild-type but not in the CYP2E1-null mice. These results support the hypothesis that genetic damage in somatic and germ cells of mice-treated with acrylamide is dependent upon metabolism of the parent compound by CYP2E1. This dependency on metabolism has implications for the assessment of human risks resulting from occupational or dietary exposure to acrylamide. CYP2E1 polymorphisms and variability in CYP2E1 activity associated with, for example, diabetes, obesity, starvation, and alcohol consumption, may result in altered metabolic efficiencies leading to differential susceptibilities to acrylamide toxicities in humans.

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PubMed2004

Subchronic acrylamide treatment induces a tissue-specific increase in DNA synthesis in the rat.

Chronic treatment with acrylamide results in increased incidence of adrenal (pheochromocytoma), testicular (mesotheliomas) and thyroid (adenoma) neoplasia in male rats. While acrylamide has been demonstrated to be DNA reactive, the tissue pattern of neoplasm induction by acrylamide suggests other mechanisms in addition to DNA reactivity may be involved in the carcinogenesis of this compound. The present studies were performed to determine whether acrylamide or an acrylamide metabolite altered cell growth in the neoplastic target tissues in the rat. DNA synthesis, mitosis and apoptosis were examined in F344 and Sprague-Dawley male rats treated with acrylamide (0, 2, or 15 mg/kg/day) for 7, 14, or 28 days. Acrylamide increased DNA synthesis in the target tissues for tumor development (thyroid, testicular mesothelium, adrenal medulla) in both rat species. In contrast, cell growth was not altered in the liver and adrenal cortex (non-target tissues for acrylamide carcinogenesis). No changes in apoptosis or mitosis were observed in any of the tissues examined. Inhibition of oxidative metabolism of acrylamide using 1-aminobenzotriazole reduced acrylamide-induced DNA synthesis only in the adrenal medulla, having no apparent effect in the testicular mesolthelium or thyroid. In summary, acrylamide produced a selective increase in DNA synthesis that correlates with the previously reported tumor target tissues.

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PubMed2005

Correlation of haemoglobin-acrylamide adducts with airborne exposure: an occupational survey.

This paper reports an occupational hygiene survey of exposure to acrylamide comparing acrylamide haemoglobin adduct measurements with personal air monitoring and glove liner analysis. The air monitoring data showed that exposure to acrylamide was well-controlled with all samples below the UK maximum exposure limit (MEL) of 300 microg/m(3) with mean exposure about one tenth of the MEL. Each worker provided two blood samples approximately 3 months apart. These samples were well correlated (r=0.61) with a slope of 0.74, indicating that exposure was reasonably constant. Mean personal airborne acrylamide levels and mean acrylamide haemoglobin adduct levels were well correlated (r=0.72, N=46) and using the calculated linear correlation, exposure at the MEL would be expected to give rise to a haemoglobin adduct level of 1,550 pmol/g globin. Smoking status did not affect the correlation. There was also a correlation between levels of acrylamide detected on gloves and haemoglobin adduct levels. A combined regression model between haemoglobin adducts, airborne acrylamide and acrylamide glove contamination was significant for both airborne acrylamide and gloves with a regression coefficient of 0.89. The study showed that haemoglobin adduct level was a good biomarker of acrylamide exposure which correlated to both inhaled and potentially skin absorbed acrylamide estimates. There was excellent discrimination between well-controlled occupational levels and environmental levels from diet and smoking, allowing haemoglobin adduct measurement to be used to determine even low level exposures. Due to the complexity of the current methodology, new techniques would be useful in making haemoglobin adducts more widely applicable.

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PubMed2003

Dietary intake of acrylamide in Sweden.

High levels of acrylamide have been found in foods heated at high temperatures, especially in carbohydrate rich foods. Several kinds of foods (industrially produced) representing different food/product groups available on the Swedish market have been analysed for acrylamide. A considerable variation in levels of acrylamide between single foodstuffs (different brands) within food categories were found, which also applies for levels in different food categories. Using recent Swedish food consumption data the dietary intake of acrylamide for the Swedish adult population was assessed based on foodstuffs with low to high levels of acrylamide (<30-2300 microg/kg), such as processed potato products, bread, breakfast cereals, biscuits, cookies, snacks and coffee. The estimated dietary intake of acrylamide per person (total population) given as the 5th, 50th and 95th percentile were 9.1, 27 and 62 microg/day respectively, from those food/product groups (mean 31 microg/day). No acrylamide was found in many other foodstuffs analysed and those were therefore not included in the dietary intake assessment of acrylamide. However, an additional minor contribution of a few microg/day of acrylamide from foods/products like poultry, meat, fish, cocoa powder and chocolates cannot be excluded. An average daily intake of 35 microg corresponds to 0.5 microg per kg body weight and day (body weight 70 kg). Risk assessments of acrylamide, made by US EPA and WHO, imply that this dietary intake of acrylamide could be associated with potential health risks.

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PubMed2003

Chemistry, biochemistry, and safety of acrylamide. A review.

Acrylamide (CH2=CH-CONH2), an industrially produced alpha,beta-unsaturated (conjugated) reactive molecule, is used worldwide to synthesize polyacrylamide. Polyacrylamide has found numerous applications as a soil conditioner, in wastewater treatment, in the cosmetic, paper, and textile industries, and in the laboratory as a solid support for the separation of proteins by electrophoresis. Because of the potential of exposure to acrylamide, effects of acrylamide in cells, tissues, animals, and humans have been extensively studied. Reports that acrylamide is present in foods formed during their processing under conditions that also induce the formation of Maillard browning products heightened interest in the chemistry, biochemistry, and safety of this vinyl compound. Because exposure of humans to acrylamide can come from both external sources and the diet, a need exists to develop a better understanding of its formation and distribution in food and its role in human health. To contribute to this effort, this integrated review presents data on the chemistry, analysis, metabolism, pharmacology, and toxicology of acrylamide. Specifically covered are the following aspects: nonfood and food sources; exposure from the environment and the diet; mechanism of formation in food from asparagine and glucose; asparagine-asparaginase relationships; Maillard browning-acrylamide relationships; quenching of protein fluorescence; biological alkylation of amino acids, peptides, proteins, and DNA by acrylamide and its epoxide metabolite glycidamide; risk assessment; neurotoxicity, reproductive toxicity, and carcinogenicity; protection against adverse effects; and possible approaches to reducing levels in food. Further research needs in each of these areas are suggested. Neurotoxicity appears to be the only documented effect of acrylamide in human epidemiological studies; reproductive toxicity, genotoxicity/clastogenicity, and carcinogenicity are potential human health risks on the basis of only animal studies. A better understanding of the chemistry and biology of pure acrylamide in general and its impact in a food matrix in particular can lead to the development of improved food processes to decrease the acrylamide content of the diet.

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PubMed2006

Effectiveness of ionizing radiation in reducing furan and acrylamide levels in foods.

Furan and acrylamide are two possible carcinogens commonly found in many thermally processed foods. The possibility of using ionizing radiation to reduce the levels of thermally induced furan and acrylamide in water and selected foods was investigated. Aqueous furan solutions, and foods (frankfurters, sausages, infant sweet potatoes) that contained furan were irradiated to various doses of gamma-rays. Water and oil spiked with acrylamide and potato chips (a known acrylamide-containing food) were also irradiated. In addition, possible irradiation-induced formation of acrylamide in glucose and asparagine solutions was analyzed. Results showed that irradiation at 1.0 kGy destroyed almost all furan in water. In frankfurters, sausages, and infant sweet potatoes, the rate of irradiation-induced destruction of furan was much lower than the rate in water, although significant reductions in furan levels were observed in all foods. Irradiation at 2.5-3.5 kGy, doses that can inactivate 5-log of most common pathogens, reduced furan levels in the food samples by 25-40%. Similarly to furan, acrylamide in water was also sensitive to irradiation. After 1.5 kGy of irradiation, most of the acrylamide was degraded. Irradiation, however, had a very limited effect on acrylamide levels in oil and in potato chips, even at a dose of 10 kGy. No detectable acrylamide was formed in the mixture of asparagine and glucose upon irradiation. These results suggest that a low dose of irradiation easily destroys furan and acrylamide in water. In real foods, however, the reduction of furan was less effective than in water, whereas the reduction in acrylamide was minimal.

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PubMed2004

Comparison of germ cell mutagenicity in male CYP2E1-null and wild-type mice treated with acrylamide: evidence supporting a glycidamide-mediated effect.

Acrylamide is an animal carcinogen and probable human carcinogen present in appreciable amounts in heated carbohydrate-rich foodstuffs. It is also a germ cell mutagen, inducing dominant lethal mutations and heritable chromosomal translocations in postmeiotic sperm of treated mice. Acrylamide's affinity for male germ cells has sometimes been overlooked in assessing its toxicity and defining human health risks. Previous investigations of acrylamide's germ cell activity in mice showed stronger effects after repeated administration of low doses compared with a single high dose, suggesting the possible involvement of a stable metabolite. A key oxidative metabolite of acrylamide is the epoxide glycidamide, generated by cytochrome P4502E1 (CYP2E1). To explore the role of CYP2E1 metabolism in the germ cell mutagenicity of acrylamide, CYP2E1-null and wild-type male mice were treated by intraperitoneal injection with 0, 12.5, 25, or 50 mg acrylamide (5 ml saline)(-1) kg(-1) day(-1) for 5 consecutive days. At defined times after exposure, males were mated to untreated B6C3F1 females. Females were killed in late gestation and uterine contents were examined. Dose-related increases in resorption moles (chromosomally aberrant embryos) and decreases in the numbers of pregnant females and the proportion of living fetuses were seen in females mated to acrylamide-treated wild-type mice. No changes in any fertility parameters were seen in females mated to acrylamide-treated CYP2E1-null mice. Our results constitute the first unequivocal demonstration that acrylamide-induced germ cell mutations in male mice require CYP2E1-mediated epoxidation of acrylamide. Thus, CYP2E1 polymorphisms in human populations, resulting in variable enzyme metabolic activities, may produce differential susceptibilities to acrylamide toxicities.

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PubMed2006

Hemoglobin adducts in the assessment of potential occupational exposure to acrylamides -- three case studies.

OBJECTIVES: Workers in three types of occupations with potential exposure to acrylamide were examined for the purpose of excluding or confirming exposure, evaluating actions for reducing exposure, or investigating the possible cause of ill health. METHODS: Workers were examined through the measurement of adducts from acrylamide (and N-methylolacrylamide) to the N-terminal valines in hemoglobin. RESULTS: The first case concerned workers transporting acrylamide-contaminated waste soil. The measured acrylamide-adduct levels were in the range of the normal background levels (ie, any potential occupational exposure was too low to be detected). The second case included workers handling a sealing product containing acrylamide and N-methylolacrylamide. One worker had an acrylamide-adduct level of 0.3 nmol/g globin, close to the level at which acrylamide-exposed persons have shown mild reversible symptoms of the peripheral nervous system. After actions to reduce exposure, the adduct levels were still elevated, and, as a precautionary measure, the sealing product was replaced. The third case concerned a man with observed neurotoxic symptoms, working with a sealing product containing acrylamide. This worker had an extremely high acrylamide-adduct level (23 nmol/g globin) (ie, the acrylamide exposure was probably the cause of his ill health). The acrylamide product was replaced, and after 5 months the adduct level had decreased to 2.4 nmol/g globin, and after another 6 months it was about 0.4 nmol/g globin. CONCLUSIONS: These studies illustrate the usefulness of in vivo dose measurement through the use of hemoglobin adducts for occupational surveillance and as a basis for the health risk assessment of electrophilically reactive compounds.

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PubMed1997

Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers, smokers and nonsmokers.

Acrylamide is a chemical which is extensively used in research laboratories for the preparation of polyacrylamide gels for electrophoresis (PAGE). Blood samples were collected from laboratory personnel who were working with PAGE, from smokers, and from nonsmokers. Hemoglobin adducts of acrylamide, acrylonitrile, and ethylene oxide were determined using the modified Edman degradation procedure. Acrylamide adducts were detected in all persons. The PAGE workers (mean 54 pmol/g) had a significantly increased adduct level compared to nonsmoking controls (mean 31 pmol/g). The acrylamide adducts in smokers (mean 116 pmol/g) correlated with the number of cigarettes smoked per day. This confirms the presence of acrylamide in tobacco smoke and shows that it is an important source of acrylamide exposure. The increased level of acrylamide adducts in the PAGE workers corresponds to an uptake of acrylamide from about 3 cigarettes per day. It is not possible from this study to draw any conclusion as to which step in the working procedure is most critical for exposure. The PAGE workers are probably not at risk for neurotoxic damage to the peripheral nervous system. However, it needs to be investigated whether the exposure to acrylamide in PAGE workers represents a risk for genotoxic and reproductive effects. The high background of acrylamide adducts in nonsmoking controls was unexpected. The origin of this background is not known. Acrylonitrile adducts were below the detection limit (< 2 pmol/g) in nonsmoking controls. In the smokers (mean 106 pmol/g) this adduct correlated with cigarettes/day and with ethylene oxide adducts. Acrylonitrile adducts could be a better indicator of tobacco smoking than ethylene oxide adducts since the latter are showing a background of endogenous origin.

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PubMed1993

Acrylamide and glycidamide impair neurite outgrowth in differentiating N1E.115 neuroblastoma without disturbing rapid bidirectional transport of organelles observed by video microscopy.

The nature of the pathogenic insult in acrylamide neuropathy is unknown, but axonal transport disturbances are suspected. Using N1E.115 neuroblastoma in vitro, we examined acrylamide and related compounds in terms of general cytotoxicity, ability to block neurite outgrowth, and effects on neurite integrity and fast axonal transport. Acrylamide, glycidamide, and methylene-bis-acrylamide were weakly cytotoxic in a 51Cr-release assay, but only at > or = 10 mM (order of efficacy: methylene-bis-acrylamide > glycidamide > acrylamide). Neurite outgrowth by differentiating cells was inhibited at 100-fold lower concentrations, with similar EC50 values for all three toxicants, i.e., acrylamide, 70 +/- 15 microM; methylene-bis-acrylamide, 92 +/- 31 microM; glycidamide, 120 +/- 30 microM. Only glycidamide (1 mM) caused degeneration of established neurites within a period of 48 h. Video-enhanced contrast differential interference contrast microscopy was used to test the effect of acrylamide and glycidamide on organelle transport in the neurites. In exposures of < or = 48 h at 1 mM, neither toxicant altered bidirectional organelle flux, measured as organelles transported per minute per micrometer of neurite diameter. Anterograde and retrograde organelle speeds were also undisturbed. These results suggest that mechanisms other than direct inhibition of organellar motility are responsible for acrylamide's neurotoxicity in vivo.

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PubMed1986

Acrylamide and iodide fluorescence quenching as a structural probe of tryptophan microenvironment in bovine lens crystallins.

Fluorescence quenching using acrylamide and iodide quenchers has been used to investigate the microenvironments of tryptophan residues in bovine alpha-, beta-, and gamma-crystallin fractions. Acrylamide quenching is very sensitive to the degree of tryptophan accessibility to the solvent containing the acrylamide. Since acrylamide is able to diffuse into the interior of the protein, accessibility to acrylamide may result from Trp residues lying at the surface of the protein or from the existence of channels leading to the interior of the protein. Iodide ion is hydrated and is limited by its large size and charge to quenching of tryptophan residues lying at or near the surface of proteins. Tryptophan residues in the lens crystallin fractions were found to be highly accessible to acrylamide, yet the rate of quenching by acrylamide was very low, indicating that the tryptophan residues of the lens crystallin fractions occupy predominately hydrophobic environments. The high accessibility to acrylamide likely results from diffusion of acrylamide into the interior of the protein. Accessibility to iodide was much lower, as was the rate of quenching by iodide, adding support to the conclusions from acrylamide quenching.

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PubMed1985

Slow axonal transport in acrylamide neuropathy: different abnormalities produced by single-dose and continuous administration.

Alterations in axonal caliber and neurofilament content have been associated with altered neurofilament transport in several models of neurofibrillary degeneration. Acrylamide intoxication provides a prototype of distal axonal degeneration, the most frequent pattern of axonal pathology in human and experimental neurotoxic injury. Neurofibrillary changes are a variable and often minor aspect of the early pathological changes observed in acrylamide intoxication, and previous studies of slow axonal transport have produced conflicting results. In this study, we have correlated slow axonal transport, specifically neurofilament transport, with structural changes in the sciatic nerve complex of rats exposed to acrylamide. To study direct toxic effects of acrylamide, young rats were given a single dose of acrylamide (75 mg/kg, i.p.). A second group received daily injections of acrylamide at a lower dose (30 mg/kg, i.p.) in order to study animals with established acrylamide neuropathy. The slow component of axonal transport was labeled by intraspinal injections of [35S] methionine. Transport of individual slow component polypeptides was compared to profiles obtained from age-matched controls. Similarly intoxicated rats were perfused for morphometric and morphological studies. Results demonstrate that two different abnormalities of the slow component of axonal transport arise at different stages during the development of experimental acrylamide neuropathy. Both patterns of altered transport have structural correlates which reflect the changes in neurofilament transport. Following a single high dose, there was a modest retardation of the leading edge of the slow component. At this time, neurofilaments accumulated in proximal axons with formation of axonal swellings. During chronic administration, when distal axonal degeneration was present, the proportion of neurofilaments in the slow component was markedly reduced, and there was prominent loss of caliber in proximal axons. We suggest that these early changes represent a direct toxic effect of acrylamide on slow transport, whereas the later changes reflect reordering of slow transport as a neuronal response to toxin-induced axonal injury. This latter effect is of sufficient magnitude to obscure the acrylamide-induced retardation of slow transport.

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PubMed2004

Dietary acrylamide and risk of renal cell cancer.

The detection of acrylamide, classified as a probable human carcinogen, in commonly consumed foods created public health alarm. Thus far, only 2 epidemiologic studies have examined the effect of dietary acrylamide on cancer risk. Presently, we reanalyzed data from a large population-based Swedish case-control study of renal cell cancer. Food frequency data were linked with national food databases on acrylamide content, and daily acrylamide intake was estimated for participants. The risk of renal cell cancer was evaluated for intake of food items with elevated acrylamide levels and for total daily acrylamide dose. Adjusting for potential confounders, there was no evidence that food items with elevated acrylamide, including coffee (OR(highest vs. lowest quartile) = 0.7; 95% CI = 0.4-1.1), crisp breads (OR(highest vs. lowest quartile) = 1.0; 95% CI = 0.6-1.6) and fried potatoes (OR(highest vs. lowest quartile) = 1.1; 95% CI = 0.7-1.7), were associated with a higher risk of renal cell cancer risk. Furthermore, there was no association between estimated daily acrylamide intake through diet and cancer risk (OR(highest vs. lowest quartile) = 1.1; 95% CI = 0.7-1.8; p for trend = 0.8). The results of this study are in line with the 2 previous studies examining dietary acrylamide and suggest there is no association between dietary acrylamide and risk of renal cell cancer.

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PubMed2005

Factors influencing acrylamide formation in gingerbread.

The influence of ingredients, additives, and process conditions on the acrylamide formation in gingerbread was investigated. The sources for reducing sugars and free asparagine were identified and the effect of different baking agents on the acrylamide formation was evaluated. Ammonium hydrogencarbonate strongly enhanced the acrylamide formation, but its N-atom was not incorporated into acrylamide, nor did acrylic acid form acrylamide in gingerbread. Acrylamide concentration and browning intensity increased both with baking time and correlated with each other. The use of sodium hydrogencarbonate as baking agent reduced the acrylamide concentration by more than 60%. Free asparagine was a limiting factor for acrylamide formation, but the acrylamide content could also be lowered by replacing reducing sugars with sucrose or by adding moderate amounts of organic acids. A significant reduction of the acrylamide content in gingerbread can be achieved by using sodium hydrogencarbonate as baking agent, minimizing free asparagine, and avoiding prolonged baking.

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