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PubMed1993

Determination of hemoglobin adducts in humans occupationally exposed to acrylamide.

Hemoglobin (Hb) adduct determinations were used to monitor occupational exposure to acrylamide (AA) and acrylonitrile (AN). Forty-one workers in a factory in the People's Republic of China who were involved in the synthesis of AA by catalytic hydration of AN and the manufacturing of polyacrylamides were studied. Ten nonexposed workers in the same city served as controls. AA and AN exposures were monitored using the modified Edman degradation procedure for the determination of their respective Hb adducts to N-terminal valine. The adduct levels in the exposed workers were 0.3-34 nmol/g Hb for AA and 0.02-66 nmol/g Hb for AN, as determined by gas chromatography-mass spectrometry (GC-MS). The formation of glycidamide (GA), the epoxide metabolite of AA, in humans was demonstrated by GC-MS analysis of its Hb adduct to N-terminal valine following acid hydrolysis, ion-exchange chromatography, and derivatization. The GA adduct was detected in samples from the exposed persons with levels of 1.6-32 nmol/g Hb. There was a linear relationship between the AA and GA adduct levels (r = 0.96) and the ratio of the in vivo doses of GA and AA was 3:10. These results suggest that AA is metabolized to GA in humans, as had previously been shown in the rat. The high AA adduct levels in the exposed workers, as compared to those expected from air concentrations, indicate that dermal exposure may contribute significantly to the total uptake of AA. The average daily in vivo doses of AA and GA in the highest exposed workers were comparable to the in vivo doses in rats injected with 3 mg/kg AA. Since a regimen of 2 mg/kg/day is known to cause a significant increase of tumors in rats, preventive measures may be necessary for humans exposed to high levels of AA in industrial settings.

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PubMed1993

Acrylamide disrupts elemental composition and water content of rat tibial nerve. III. Recovery.

We have previously demonstrated that subacute and subchronic acrylamide (ACR) intoxication are associated with a loss of subcellular elemental regulation in myelinated axons and Schwann cells of rat tibial nerve (LoPachin et al., Toxicol. Appl. Pharmacol. 115, 21-34, 1992; LoPachin et al., Toxicol. Appl. Pharmacol. 115, 35-43, 1992). In the present study, rats were allowed to recover partially from subchronic oral ACR intoxication (2.8 mM in drinking water for approximately 30 days). Elemental composition and water content of tibial nerve myelinated axons and Schwann cells were measured by electron probe X-ray microanalysis. Results show that K and Cl concentrations in larger tibial nerve axons were shifted toward normal values or above. For the most part, small axons also exhibited elemental changes that reflected recovery from ACR intoxication. Mitochondria displayed elemental changes that were similar to corresponding axoplasm. Schwann cells in tibial nerve of recovering animals had altered Na, P, Cl, K, and Mg concentrations that were similar in magnitude and extent to those occurring during ACR intoxication. In contrast, myelin displayed few changes. These results suggest that the recovery process following ACR intoxication is associated with characteristic changes in subaxonal elemental composition that might be related to repair mechanisms. That recovery-related elemental changes differ from those associated with intoxication provides additional support for the hypothesis (LoPachin et al., Toxicol. Appl. Pharmacol. 115, 21-34, 1992) that perturbation of elemental regulation is a specific component of ACR neurotoxicity. The observation of persistent Schwann cell disruption during recovery might reflect either long-term secondary consequences or delayed recovery from direct injury. Further studies are necessary to resolve this issue.

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PubMed1996

The effects of 2,5-hexanedione and acrylamide on myosin heavy chain isoforms of slow and fast skeletal muscles of the rat.

We examined the effects of 2,5-hexanedione (2,5-HD) and acrylamide (ACR) on the muscle fiber types and myosin heavy chain (MHC) isoform composition of the slow-twitch soleus and fast-twitch plantaris muscles of rats. We employed two differently designed experiments with respect to the dosage levels and treatment periods for developing clinical neuropathies. When male Wistar rats were subcutaneously injected with 4.5 mmol of 2,5-HD/kg or 0.4 mmol of ACR/kg, 5 days a week, they developed paralysis of the hindlimbs in 4 weeks (high-dosage experiment). When they were subcutaneously injected with 3.5 mmol of 2,5-HD/kg or 0.35 mmol of ACR/kg, 5 days a week, paralysis of the hindlimbs did not develop until 6 weeks (low-dosage experiment). We examined mainly the rats treated with the neurotoxicants for 4 and 8 weeks in the high-and low-dosage experiments, respectively. Significant decreases in the maximum motor conduction velocity of the sciatic nerves were observed in the hindlimbs of the rats in both experiments. The weights of the soleus and plantaris muscles were significantly reduced in the 2,5-HD-treated rats in both experiments, while in the ACR-treated rats, the weights of both muscles decreased only in the low-dosage experiment. We could not detect any changes in the fiber type composition of the muscles by any of the treatments. However, biochemical analysis revealed decreases in the values (percentage) of the relative amounts of fast-type MHC IIa and IIb isoforms to total MHC isoforms in the 2,5-HD-treated rats, but not in the ACR-treated rats in the high-dosage experiment. In contrast, significant differences in the relative amounts of MHC isoforms were not observed after administration of the low dosage of 2,5-HD. These results suggest that 2,5-HD preferentially disorders the muscle fibers which contain the MHC II isoform. These effects may occur only after the relatively acute intoxication of 2,5-HD at a high dosage.

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PubMed1998

Biochemical and morphologic characterization of acrylamide peripheral neuropathy.

To determine whether reduced Na+/K+-ATPase activity might be involved in acrylamide (ACR)-induced peripheral axon swelling and degeneration, rubidium (Rb+) transport was measured as an index of enzyme function. x-ray microanalysis was used to quantify elemental Rb uptake and accumulation in internodal myelinated axons, mitochondria, Schwann cells, and myelin of rat tibial nerve cryosections. Results demonstrated impairment of Rb uptake in tibial axons from orally intoxicated (2.8 mM ACR for 34 days), moderately affected rats. In severely affected oral rats (49 days), complete inhibition of Rb transport and frank axon degeneration were evident. However, in moderate-to-severely affected rats exposed to ACR via ip injection (50 mg/kg/day for 11 days), neither structural nor enzymatic changes were present in tibial fibers. These findings in nerve cryosections suggested inhibition of axolemmal Na+ pump activity and degeneration were dependent upon route of ACR administration. This possibility was substantiated by a quantitative longitudinal morphometric study of conventionally fixed tibial nerve. Oral ACR treatment (2.8 mM ACR for 15-49 days) was associated with progressive axon degeneration, which was preceded by atrophy. Axonal swellings were rarely (<1%) observed. In contrast, ip ACR injection (50 mg/kg/day for 5-11 days) produced classic behavioral neurotoxicity but did not alter axon morphology in tibial nerve. Thus, fiber degeneration and decreased Na+ pump activity were consequences of subchronic oral ACR administration. This parallel expression suggests a mechanistic relationship. However, the corresponding general neurotoxicological significance is unclear since, behavioral toxicity induced by ip ACR develops without structural and enzymatic changes in tibial nerve.

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PubMed2005

Acrylamide neurotoxicity: neurological, morhological and molecular endpoints in animal models.

Acrylamide (AA) monomer is used in numerous chemical industries and is a contaminant in potato- and grain-based foods prepared at high temperatures. Although experimental animal studies have implicated carcinogenicity and reproductive toxicity as possible consequences of exposure, neurotoxicity is the only outcome identified by epidemiological studies of occupationally exposed human populations. Neurotoxicity in both humans and laboratory animals is characterized by ataxia and distal skeletal muscle weakness. Early neuropathological studies suggested that AA neurotoxicity was mediated by distal axon degeneration. However, more recent electrophysiological and quantitative morphometric analyses have identified nerve terminals as primary sites of AA action. A resulting defect in neurotransmitter release appears to be the pathophysiological basis of the developing neurotoxicity. Corresponding mechanistic research suggests that AA impairs release by adducting cysteine residues on functionally important presynaptic proteins. In this publication we provide an overview of recent advances in AA research. This includes a discussion of the cumulative nature of AA neurotoxicity and the putative sites and molecular mechanisms of action.

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PubMed1995

Acrylamide-induced peripheral neuropathy in normal and neurofilament-deficient Japanese quails.

Morphological effects of acrylamide (AC) on the peripheral nerves in normal and neurofilament (NF)-deficient (Quv) Japanese quails were investigated. AC (100 mg/kg) was injected intraperitoneally every other day. After the birds manifested neurological signs, they were necropsied (after 10 approximately 21 AC injections) and the sciatic and tibial nerves were examined. In both normal and Quv qualis, AC produced axonopathy with a distal-proximal progression. In AC-intoxicated normal quails, the nerve fiber pathology was characterized by typical Wallerian-like degeneration, consisting of axonal degeneration, myelin breakdown, macrophage migration. Schwann cell proliferation and regeneration of nerve fibers. Ultrastructurally, AC-induced NF accumulation was detected in the axon of myelinated nerve fibers. In AC-intoxicated Quv qualis, axonal degeneration with accumulation of membranous organelles occurred; however, sequential events of Wallerian-like degeneration were not as prominent as in AC-intoxicated normal qualis. These results demonstrated that NF-deficient Quv quails are sensitive to neurotoxic effects of AC. On the other hand, the different pathology of AC-intoxicated normal and Quv qualis indicates the presence or absence of NFs influences the appearance and extent of AC axonopathy.

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PubMed1995

Use of sialylated or sulfated derivatives and acrylamide copolymers of Gal beta 1,3GalNAc alpha- and GalNAc alpha- to determine the specificities of blood group T- and Tn-specific lectins and the copolymers to measure anti-T and anti-Tn antibody levels in cancer patients.

Sialylated or sulfated derivatives and acrylamide copolymers of blood group T-(Gal beta 1,3GalNAc alpha-) and Tn-(GalNAc alpha) haptens were studied for their interaction with the lectins of peanut (PNA), Agaricus bisporus-(ABA), Helix pomatia-(HPA) and Vicia villosa B4-(VVA), using asialo Cowper's gland mucin (ACGM), which contains both T and Tn epitopes, as the coating substrate in enzyme linked lectin assay. Both T and Tn copolymers (-40 haptens) showed high affinity and strict specificity; although the T-copolymer at 0.05-0.07 microM concentration caused 50% inhibition of interaction of either PNA or ABA with ACGM, there was little inhibition of the HPA and VVA interactions even at over 100 times that concentration. The Tn-copolymer at 0.02-0.05 microM inhibited HPA or VVA interaction with ACGM by 50% but gave virtually no inhibition of PNA and ABA binding. Sialyl, sulfate or methyl group substitution on C-6 of GalNAc of the T-haptene did not prevent interaction with PNA but almost abolished interaction with ABA. In contrast, sialyl or sulfate group on C-6 and sulfate on C-3 of Gal in Gal beta 1,3GalNAc alpha- inhibited almost completely the interaction of PNA with ACGM but had only a slight effect on the interaction of ABA; C-6 substitution with either sialic acid or sulfate on GalNAc alpha- almost abolished the interaction of both HPA and VVA with ACGM.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1992

Somatofugal axonal atrophy precedes development of axonal degeneration in acrylamide neuropathy.

Somatofugal axonal atrophy is part of the neuronal perikaryal response to axonal injury (axon reaction). Chronic administration of acrylamide (AC) produces proximal atrophy in virtually all sensory fibers in lumbar dorsal root ganglion (DRG) despite the presence of many intact axons in the distal portion of the sciatic nerve. This suggests that the development of axonal atrophy in AC-intoxicated animals is not solely due to a toxic chemical-induced axonal degeneration (axotomy). In this study, we asked whether axonal atrophy arises before onset of axonal degeneration. Rats were given a single intraperitoneal (i.p.) high dose of AC (75 mg/kg), which blocks retrograde axonal transport, followed by daily intraperitoneal injections (30 mg/kg, for 4 days). At 5 days, sensory fibers in the L4 and L5 DRG appeared smaller in caliber and less circular in shape compared to fibers from age-matched normal animals. Axonal diameters of sensory fibers in the L5 dorsal root were significantly (p less than 0.05) reduced at distances up to 2 mm from the DRG. Quantitative electron microscopy demonstrated that the reduction in caliber was due to a decreased neurofilament (NF) content. Axonal degeneration was not present in the distal portion of both centrally (dorsal root) and peripherally (sciatic nerve) projecting sensory fibers at this time, although primary afferent terminals in muscles of the hindfeet were packed with NFs. The somatofugal progression of the atrophy was evident following more prolonged exposures (10-28 days). It is suggested that AC produces somatofugal axonal atrophy by inhibiting the delivery of a retrogradely transported target-derived "trophic" signal to the neuronal perikaryon.

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PubMed1990

Drying acrylamide slab gels for fluorography without using gel drier and vacuum pump.

A method for drying acrylamide slab gels for fluorography without using a gel drier and a vacuum pump is described. The method involves the use of inexpensive acrylic frames, cellophane, and plastic supplies. The fluorographs obtained from gels dried by this method are comparable to those obtained using a gel drier and a vacuum pump. Several gels can be dried by this method simultaneously at room temperature. The method is less time consuming and is economical and practically crack free.

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PubMed1986

Selective acrylamide-induced degeneration of color opponent ganglion cells in macaques.

P beta (color opponent) retinal ganglion cells in macaques were found to degenerate as a result of oral administration of acrylamide. Histological examination, wheat germ agglutinin-horseradish peroxidase transport and cytochrome oxidase histochemistry indicate that other retinal ganglion cells and other neurons in the visual pathways were spared.

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PubMed1994

The spermatid micronucleus test with the dissection technique detects the germ cell mutagenicity of acrylamide in rat meiotic cells.

As a part of the development and validation of the spermatid micronucleus test (SMNT) in the project 'Detection of Germ Cell Mutagens' sponsored by the CEC we studied the mutagenicity of acrylamide (AA) and mitomycin C (MMC). Of two alternative techniques, we used the 'dissection technique' based on microdissection of seminiferous tubules offering a narrow window for evaluation of cell stage sensitivity, and including DNA-specific staining and scoring. AA given as a single injection of 50 or 100 mg/kg did not significantly increase MN frequencies. When a subchronic treatment (4 x 50 mg/kg) was given, a significant increase over background was observed 18 and 19 days after the last injection, indicating genotoxic activity in preleptotene spermatocytes and late spermatogonial stages. MMC given as single injections of 0.5 or 1.0 mg/kg increased MN frequencies significantly 17, 18, 19 and 20 days after treatment as a result of clastogenicity in S phase cells. DNA flow cytometry did not show cytotoxicity of AA to preleptotene spermatocytes, but a small decrease in the numbers of stem cells. If spindle disturbances are caused by AA, as suggested, they were not detectable by induction of spermatid MN in vivo 1 or 3 days after treatment or by treatment with AA of cultured segments of seminiferous tubules undergoing meiotic divisions in vitro. In conclusion, the SMNT with the dissection technique is able to show the germ cell clastogenicity of AA and MMC. AA was observed to have a much weaker MN inducing potency than MMC.

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PubMed1994

Weak genotoxicity of acrylamide on premeiotic and somatic cells of the mouse.

The effects of acrylamide (AA) were evaluated, under the EEC/STEP project 'Detection of Germ Cell Mutagens', by carrying out several cytogenetic assays on mouse germ and somatic cells. The spermatid micronucleus (MN) test was applied after treatment of meiotically dividing or premeiotic S phase cells. Acute treatments (50 and 100 mg/kg i.p.) as well as subchronic exposure to AA (4 x 50 mg/kg, 4 i.p. injections at 24-h intervals) were performed. A weak increase of MN was induced only by treatment with AA of cells in S phase. Sister-chromatid exchange (SCE) analysis in differentiating spermatogonia treated i.p. with 50 and 100 mg/kg confirmed the weak genotoxicity of AA in the premeiotic stages of spermatogenesis. The application of the MN test in peripheral blood reticulocytes of the same animals used for the spermatid MN assay indicated that the cytogenetic effects induced by AA in the somatic and the germ cell lines are comparable in magnitude. The results obtained in this study by applying the spermatid micronucleus assay are in very good agreement with those reported by two other laboratories with the same technique.

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PubMed1994

Acrylamide-induced chromosomal damage in male mouse germ cells detected by cytogenetic analysis of one-cell zygotes.

Within a project coordinated by the Commission of the European Communities for the detection of germ cell mutagens, the cytogenetic analysis of first-cleavage metaphases was carried out to detect chromosomal damage induced by acrylamide (AA) in meiotic and postmeiotic stages of mouse spermatogenesis. Male mice were intraperitoneally injected with single acute doses of 75 or 125 mg/kg or treated with five daily injections of 50 mg/kg and mated either 7 or 28 days after the end of treatment. Chromosomal aberrations were scored in C-banded metaphases prepared from one-cell zygotes by a mass harvest technique. AA treatment of late spermatids-spermatozoa resulted in significant increases of structural aberrations at all doses tested. The data could be fitted to a curvilinear regression and a doubling dose of 23 mg/kg was calculated. The large majority of observed aberrations were of the chromosome type, including dicentrics, rings and translocations, in agreement with a mechanism of chromosomal damage mediated through the alkylation of DNA-associated protamines. Even though the frequency of aberrations 28 days after treatment was not significantly higher than the control value, the presence of multiple rearrangements in two cells suggested that AA might also have a minor effect on spermatocytes. The results of the cytogenetic analysis of first cleavage metaphases agreed well both qualitatively and quantitatively with the outcome of dominant lethal and heritable translocation assays. AA-induced cytotoxicity was monitored by flow cytometric DNA content analysis of testicular cells. By this method, a dose-dependent depletion of mature spermatids after treatment of spermatogonia and a toxic effect upon primary spermatocytes were detected.

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PubMed1995

EC/US workshop report: assessment of genetic risks associated with exposure to ethylene oxide, acrylamide, 1,3-butadiene and cyclophosphamide.

The EC/US Workshop on Risk Assessment: 'Human Genetic Risks from Exposure to Chemicals, Focusing on the Feasibility of a Parallelogram Approach' had as its main objective the identification of the methodology, data requirements and mechanistic research to understand the human health impact of germ cell mutagens. Specifically, it represented an evaluation of current knowledge and the identification of future research needs for a more precise assessment of human genetic risks from exposure to mutagenic chemicals. Four chemicals were selected for review at the Workshop and in this Special Issue: ethylene oxide, 1,3-butadiene, acrylamide, and cyclophosphamide. The first three are important industrial chemicals with substantial use worldwide and, therefore, considerable potential for human exposure. The fourth, cyclophosphamide, is a commonly used cancer chemotherapeutic agent. This Special Issue contains the major scientific reports from the workshop. These include four Introductory Papers (on the parallelogram concept, alternative genetic risk assessment approaches, regulatory data needs, and the research background for risk assessment of ethylene oxide), four Working Group Reports on the specific compounds mentioned above and, finally, three Crosscutting Papers pertinent to the issue of germ-line mutagenesis and genetic risk estimation.

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PubMed1985

Acrylamide preferentially affects slowly adapting cutaneous mechanoreceptors.

Acrylamide (ACR) is a vinyl monomer which produces a distal axonopathy. Several investigators have shown that ACR produces deficits in proprioception. This deficit appears to result in part from altered muscle spindle function. ACR also produces deficits in cutaneous sensory perception. The purpose of these experiments was to determine whether ACR alters cutaneous sensory receptors. Cats were administered ACR (30 mg/kg) for either 3, 5, or 10 days. Following the last injection, the tibial nerve was isolated and four different mechanoreceptor types were isolated. These were field, rapid adapting (RA), and slowly adapting type 1 and type 2. The frequency response of the slowly adapting receptors was normal. However, the number of slowly adapting receptors identified was significantly reduced in all three ACR-treated groups. There was also a decrease in the number of field receptors after 10 day ACR administration. The total number of receptors per tibial nerve was unchanged in the ACR 3- and ACR 5-day groups but was significantly reduced in the ACR 10-day group. These data show a preferential effect of ACR on slowly adapting receptors early in the neuropathy. However, the reduction in field receptors and the total number of receptors at 10 days suggests that ACR eventually affects all mechanoreceptors in the tibial nerve.

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PubMed1987

Primary afferent terminal function following acrylamide: alterations in the dorsal root potential and reflex.

The dorsal root potential (DRP) and the dorsal root reflex (DRR) were studied in acrylamide (ACR)-induced axonopathy to determine the nature and extent of primary afferent terminal (PAT) dysfunction. Cats were administered 30 mg/kg/day ACR for either 5 (ACR 5D) or 10 (ACR 10D) days. The day after the last injection, the spinal cord as isolated in situ and the DRP and DRR were elicited. It was found that only 21% of the ACR 10D animals exhibited a DRP. Furthermore, in that 21%, the DRP appeared to degrade over distance differently from the control group. There was no change in the DRP evoked in the ACR 5D group. ACR affected the DRR when evoked from the cutaneous sural nerve (SU) to a greater extent than when evoked from the medial gastrocnemius (MG) nerve. A SU-evoked DRR could not be elicited in any of the animals in the ACR 10D group and in only 20% of the ACR 5D group. There was no difference in the ability to elicit a MG-evoked DDR in either ACR-treated group when compared to control. However, the maximum-evoked area under the DRR elicited from the MG nerve was significantly smaller in the ACR-treated groups than in control. These data show that ACR does indeed impair PAT function. ACR preferentially affects the PAT processing of the SU when compared to the MG nerve, which may indicate that the selective vulnerability of the largest diameter fibers to ACR is not necessarily true.

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PubMed1991

Toxic neurofilamentous axonopathies and fast anterograde axonal transport. III. Recovery from single injections and multiple dosing effects of acrylamide and 2,5-hexanedione.

Fast anterograde axonal transport has been advanced as a potential site of action of acrylamide (ACR) and the neurotoxic gamma-diketones in producing nerve degeneration. The segmental analysis method of axonal transport was used to measure the rate and quantity of protein transport in the rat sciatic nerve from 1 to 24 hr after a single injection of 50 mg/kg (0.7 mmol/kg) ACR or 4 mmol/kg 2,5-hexanedione (2,5-HD). The single injection of ACR or 2,5-HD resulted in an immediate reduction in transport quantity of 48 and 43%, respectively. Transport remained depressed for 16 hr; recovery occurred from 16 to 24 hr reaching control levels at 24 hr postinjection for both toxicants. Protein transport, measured immediately after the 2nd, 4th, 7th, and 10th injections, was reduced 36-38% by 50 mg/kg ACR and 30-43% by 4 mmol/kg 2,5-HD. Therefore, both ACR and 2,5-HD produce a transient and repeated compromise of fast anterograde transport during the dosing regimen which results in distal nerve degeneration. Assuming a rate of recovery after each subsequent dose similar to the first, the protein delivery to the axon was calculated to be reduced 29% by ACR and 22% by 2,5-HD. Current evidence supports the hypothesis that a toxicant-induced reduction in protein delivery to the axon by ACR and 2,5-HD contributes to development of axonal degeneration.

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PubMed1992

Acrylamide disrupts elemental composition and water content of rat tibial nerve. I. Myelinated axons.

The mechanism by which acrylamide (ACR) produces distal axonopathy in humans and laboratory animals is unknown. The possibility that this neuropathy involves deregulation of elements and water in rat peripheral nerve has been investigated. Electron probe X-ray microanalysis was used to measure percentages of water and concentrations (mmol element/kg dry or wet wt) of Na, P, S, Cl, K, Ca, and Mg in axoplasm and mitochondrial areas of tibial nerve axons. Results show that when rats were intoxicated with ACR by either the oral (2.8 mM in drinking water, up to 60 days) or the intraperitoneal (ip, 50 mg/kg/day x 5 or 10 days) route, a progressive loss of internodal axoplasmic K, Cl, and Na regulation was observed in subpopulations of myelinated fibers. Elemental deregulation was manifest as a shift in mean elemental content, widening of the corresponding concentration range, and a statistically significant increase in data variance. In internodal axonal regions, elemental composition of mitochondrial areas was not altered by ip ACR intoxication, whereas oral exposure was associated with delayed changes in Na, K, Cl, Ca, and Mg. In swollen axons, axoplasm and mitochondrial areas exhibited complete loss of element and water compartmentalization. This global decompartmentalization of swollen axons was quantitatively similar regardless of the route or length of ACR exposure. The results of this study suggest that a progressive loss of elemental regulation in axoplasm of myelinated tibial nerve fibers might be mechanistically related to ACR neurotoxicity.

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