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PubMed1990

Baroreceptor dysfunction in acrylamide axonal neuropathy.

Clinical studies suggest that baroreceptor dysfunction may occur in peripheral neuropathies but this abnormality has never been observed directly or characterized. Carotid sinus nerve and depressor nerve activity was recorded in rabbits with a mild axonal neuropathy produced by acrylamide. Arterial pressure was changed by altering intravascular volume. The pattern of baroreceptor discharge in the affected animals was always different, there being a marked reduction of diastolic phase nerve activity at normal arterial pressures. In addition, nerve activity in both baroreceptor nerves was significantly reduced. The thresholds of aortic arch baroreceptors were elevated and aortic arch baroreceptor activity was less than carotid sinus baroreceptor activity at lower arterial pressures. In acrylamide axonal neuropathy, even when mild, there is baroreceptor dysfunction.

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PubMed1983

Acrylamide fluorescence quenching studies on the actin-induced change in protein dynamics in the subfragment-1/subfragment-2 link region of cardiac myosin.

In order to obtain information about the actin-induced conformational change around the subfragment-1/subfragment-2 link region of myosin, measurements of the fluorescence quenching by acrylamide were made on cardiac myosin and its heavy meromyosin, in which the reactive lysyl residue located in the link region was labeled with an extrinsic fluorophore, the N-methyl-2-anilino-6-naphthalenesulfonyl group. The results with the model compound indicated the involvement of a collisional quenching mechanism for the fluorophore. The quenching rate constant calculated from measured quenching constants using available lifetime data was extremely low for the labeled myosin (0.59 X 10(8) M-1 . S-1), suggesting that the fluorophore bound to myosin is surrounded by segments of proteins. This value was independent of the solvent viscosity, indicating that the quenching reaction is limited by fluctuations in the protein matrix, which produce the inward movement of acrylamide. Chymotryptic digestion of the labeled myosin, which yielded the light chain-2-deficient heavy meromyosin, made the bound fluorophore slightly exposed. Addition of F-actin resulted in about 40% reduction in the quenching rate constants for the labeled myosin and heavy meromyosin. The actin effect was reversed by adding ATP. These results suggest that the binding of actin to myosin makes the protein matrix around the subfragment-1/subfragment-2 link region less mobile.

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PubMed1994

Acrylamide-induced neurotoxicity in the central nervous system of Japanese quails. Comparative studies of normal and neurofilament-deficient quails.

Acrylamide (AC) neurotoxicity in the central nervous system (CNS) in normal and neurofilament (NF)-deficient mutant (Quv) Japanese quails was investigated. Acrylamide (100 mg/kg) was injected intraperitoneally every other day. After the birds manifested neurological signs, they were necropsied (after 10-30 AC injections) and examined morphologically. All of the AC-intoxicated normal quails showed distal, retrograde nerve fiber degeneration associated with neurofilamentous axonal swellings in the spinal nerve tracts. There were axonal swellings without degenerative changes in other parts of the CNS. In Quv quails, distal nerve fiber degeneration was not observed in the spinal nerve tracts, although AC-induced membranous organelle accumulations were found in preterminal and terminal nerve fibers. Cytological remodeling similar to the axon reaction was seen mainly in dorsal root ganglia of AC-intoxicated normal and Quv quails. In addition, perikaryal response indicating impaired metabolic activity was observed in Quv quails. The present study showed that Quv quails are sensitive to neurotoxic effects of AC. It is suggested that AC-induced neurotoxicity is not initiated exclusively through its action on NF.

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PubMedDate not supplied

The evolution of intracellular responses to acrylamide in rat spinal ganglion neurons.

Acrylamide (30 mg or 50 mg/kg/day, 5 days each week) was injected intraperitoneally into rats for up to 4 weeks. Lumbar spinal ganglia, spinal cord and lumbrical muscle spindles were examined by light and electron microscopy at various times during this period. The first abnormalities in spinal ganglion neurons were seen at 7 days when an apparent increase in numbers of mitochondria, some being hypertrophic, were found in a few large light cells. This was 10 days before any significant Wallerian degeneration was found in muscle spindle sensory fibres. Mitochondrial changes became more marked with time and were later associated with RER disruption, loss of neurofilaments and peripheral displacement of the nucleus thus mimicking chromatolysis of the axon reaction. All these changes began, however, before axon degeneration. Evidence of increased satellite cell activity was maximal at 21 days. These changes are discussed in the light of the possibility that calcium entry into the cell may be seriously increased early in the intoxication as a direct result of the presence of acrylamide and that many of these cellular features are secondary responses to such an event. Distal degeneration of axons seems likely to be secondary to the perikaryal changes.

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PubMed1988

A comparison of the effects of acrylamide and experimental diabetes on the retrograde axonal transport of proteins in the rat sciatic nerve: analysis by two-dimensional polyacrylamide gel electrophoresis.

Retrogradely transported proteins that accumulated for 18 h distal to a ligature on the sciatic nerve of rats were separated by two-dimensional polyacrylamide gel electrophoresis and visualised with silver stain. A total of 14 proteins were detectable in this way as being retrogradely transported. In rats rendered diabetic 14 days previously by a single intravenous dose of streptozotocin, the accumulation of four of those proteins was noticeably decreased. Administration of acrylamide to a cumulative dose of 150 mg.kg-1 or 350 mg.kg-1 decreased the accumulation of four and eight proteins, respectively. Three of the four protein changes were common to the diabetic and acrylamide-treated animals, and were present before signs of neuropathy could be detected. The results suggest that those alterations may play a causal role in the development of neuropathy.

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PubMed1985

Autoradiographic changes of 3H-alpha-bungarotoxin binding in rat hind limb muscles after a cryoinjury of the sciatic nerve and in acrylamide intoxication.

The morphological distribution of acetylcholine receptors in rat tibialis anterior and soleus muscles after a cryoinjury of the sciatic nerve was studied by in vitro autoradiography with 3H-alpha-bungarotoxin (3H-alpha-Btx). Tibialis anterior from rats intoxicated with acrylamide was also investigated by this technique. A computer system was used for densitometry and colour coding of the autoradiographs. In normal muscle, 3H-alpha-Btx binding was observed only at the motor endplates. From the second day after the nerve lesion the area of binding spread from the motor endplate region towards the muscle-tendon regions and on the 16th day almost all parts of the muscles showed increased binding. The binding had begun to decrease in the middle parts of the muscles on the 20th day and on the 30th day binding was observed only in the motor endplate area. Tibialis anterior from rats intoxicated with acrylamide (total dose 1100 mg X kg-1) showed 3H-alpha-Btx binding over the entire muscle.

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PubMed1994

Purification and characterization of an amidase from an acrylamide-degrading Rhodococcus sp.

A constitutively expressed aliphatic amidase from a Rhodococcus sp. catalyzing acrylamide deamination was purified to electrophoretic homogeneity. The molecular weight of the native enzyme was estimated to be 360,000. Upon sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the purified preparation yielded a homogeneous protein band having an apparent molecular weight of about 44,500. The amidase had pH and temperature optima of 8.5 and 40 degrees C, respectively, and its isoelectric point was pH 4.0. The amidase had apparent K(m) values of 1.2, 2.6, 3.0, 2.7, and 5.0 mM for acrylamide, acetamide, butyramide, propionamide, and isobutyramide, respectively. Inductively coupled plasma-atomic emission spectometry analysis indicated that the enzyme contains 8 mol of iron per mol of the native enzyme. No labile sulfide was detected. The amidase activity was enhanced by, but not dependent on Fe(2+), Ba(2+), and Cr(2+). However, the enzyme activity was partially inhibited by Mg(2+) and totally inhibited in the presence of Ni(2+), Hg(2+), Cu(2+), Co(2+), specific iron chelators, and thiol blocking reagents. The NH2-terminal sequence of the first 18 amino acids displayed 88% homology to the aliphatic amidase of Brevibacterium sp. strain R312.

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PubMed1981

Megaoesophagus due to acrylamide neuropathy.

Greyhound dogs exposed to oral acrylamide for a period of eight weeks developed a sensorimotor peripheral neuropathy that had many features in common with acrylamide neuropathy seen in other species. Most of the animals also developed the clinical and radiological features of megaoesophagus. The association of neuropathy and megaoesophagus suggests that an axonopathy of the vagus may be an aetiological factor in this disorder.

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PubMed1985

Low temperature and acrylamide inhibit lens opacification caused by calcium.

We studied lens opacification of rabbit lenses in culture. Opacification was produced by maintaining rabbit lenses in medium containing calcium concentrations as high as 10 mmol/l and the opacity was measured using LASER spectroscopy. Increasing calcium caused significant opacification in lens cortex while the transparency in lens nucleus was unchanged by these concentrations. The cortical opacity was inhibited by low temperature and acrylamide. The maximum inhibition of opacity occurred at a concentration of 1% acrylamide and a temperature of 4 degrees C. The opacification due to a phase separation in nuclear cells was unaffected by these concentrations of calcium.

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PubMed1992

Inactivation of placental factor XIIIa by acrylamide.

Acrylamide rapidly and irreversibly inactivates thrombin activated Factor XIIIa, without affecting neither the intact zymogen nor its proteolytic activation. The inactivation is strictly dependent on the presence of calcium ions and is accompanied by a decrease in the number of free and total thiol residues, suggesting that cysteine residue(s), whose reactivity is modulated by calcium, is (are) probably responsible for the acrylamide-directed inactivation.

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PubMed2004

Effects on the peripheral nervous system of tunnel workers exposed to acrylamide and N-methylolacrylamide.

OBJECTIVES: This study evaluates the possible toxic effects on the peripheral nervous system of tunnel workers exposed to acrylamide and N-methylolacrylamide during grouting work. METHODS: Symptoms and nerve conduction velocities (NCV) were recorded for 24 tunnel workers 4 and 16 months after the cessation of exposure during grouting operations. Fifty tunnel workers not involved in grouting operations served as referents. Exposure was assessed by questionnaires, qualitative exposure indices, and measurements of hemoglobin adducts after the cessation of exposure. RESULTS: The exposed workers reported a higher prevalence of symptoms during grouting work than they did in an examination 16 months later. A statistically significant reduction in the mean sensory NCV of the ulnar nerve was observed 4 months postexposure when compared with the values of the reference group (52.3 versus 58.9 m/s, P = 0.001), and the mean ulnar distal delay was prolonged (3.1 versus 2.5 ms, P = 0.001). Both measures were significantly improved when measured 1 year later. Exposure-related improvements were observed from 4 to 16 months postexposure for both the median (motor and sensory NCV and F-response) and ulnar (sensory NCV, F-response) nerves. A significant reversible reduction in the mean sensory amplitude of the median nerve was also observed, while the mean sensory amplitude of the sural nerve was significantly reduced after 16 months. CONCLUSIONS: The results indicate demyelinating and axonal changes in peripheral nerves of tunnel workers in relation to exposure to N-methylolacrylamide and acrylamide during grouting operations. The changes were slight, mostly subclinical, and most of the effects were reversible, with normalization after 1 year.

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PubMed2002

Acrylamide and N-methylolacrylamide poisoning in a herd of Charolais crossbreed cattle.

Seven beef cattle from a herd accidentally exposed to acrylamide and N-methylolacrylamide while grazing were observed for eight months. They showed clinical signs of impaired nerve function, mainly in the hindlegs, with varying degrees of weakness and ataxia. The animals were irritable, nervous and hypersensitive to touch. Both pupils of the most badly affected animal were dilated and it had poor pupillary light responses; it also showed signs of axonal neuropathy. Selected haematological and clinical chemistry variables were normal. The severity of the neurological signs was correlated with the concentrations of haemoglobin adducts of acrylamides. The animals recovered substantially after their exposure. The gestations of four of the animals which were in calf proceeded normally.

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PubMed1992

Studies on biochemical mechanism of neurotoxicity induced by acrylamide in rats.

The effects of acrylamide on calmodulin (CaM), cAMP, cGMP, Ca2+, Mg(2+)-ATPase and 45Ca2+ uptake in nervous system were determined in Wistar rats (ip, 10 or 50 mg.kg-1 for 12 d). The results indicate that acrylamide caused an alteration in calcium homeostasis in rat brain by decreasing the Ca(2+)-sequestering capacity of microsomes, and this may occur due to an efflux of calcium secondary to a microsomal structure damage. The changes of CaM in nervous system coupled with potential alteration in the intracellular Ca2+ concentration could affect many CaM-dependent enzymes (i.e. Ca2+, Mg(2+)-ATPase) and cyclic AMP system, and CaM or cAMP is known to be "toxicological second messenger" that could initiate neurotoxicity, though more work is needed to elucidate the details of the mechanism.

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PubMedDate not supplied

Overview of acrylamide monitoring databases.

Since high acrylamide levels in carbohydrate-rich food were reported in 2002, many research activities were started in order to gain knowledge on occurrence, formation, and prevention of this compound in food products. Among them, monitoring programs were conducted in many countries worldwide by official bodies as well as by the food industry. National and international bodies set up monitoring databases. In 2003, both the European Commission and the World Health Organization posted calls for data and placed their spreadsheets for the submission of data on the Web. The goal of the databases is to collect data for a reliable estimation of the exposure of consumers to acrylamide via the food chain. This paper describes the assessment of the data quality and outlines the composition of the data in the 2 databases, to date.

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PubMedDate not supplied

Acrylamide analysis: assessment of results from six rounds of Food Analysis Performance Assessment Scheme (FAPAS) proficiency testing.

Six proficiency tests have now been completed in an ongoing program of the UK Food Analysis Performance Assessment Scheme (FAPAS) for the analysis of acrylamide in a range of food matrixes. Homogeneous test material samples were requested by laboratories throughout the world, with 29 to 45 submitting results for each test. Results were analyzed by appropriate statistical procedures, and z-scores were awarded for reported values. In the absence of both legislation and collaborative trial data, the target standard deviation was derived from the Horwitz equation, although it is acknowledged that there is a need to establish a "fit for purpose" target standard deviation specifically for acrylamide analysis. Participants were encouraged to use the analytical method routinely used in their own laboratory and to provide details of their procedure. Close examination of the data submitted indicates that performance is generally acceptable in terms of accuracy. There is no significant difference between results submitted by gas chromatography and liquid chromatography (GC and LC) methods, and no method dependency on the use of internal standards or sample size. However, choice of extraction solvent may be important, with indications that plain water is an acceptable extraction method. There is evidence from the most recent test that direct (underivatized) GC methodology may present problems, but more data are required and this aspect will be monitored in the continuing proficiency testing program.

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PubMed1990

The distribution of [14C]acrylamide in rainbow trout studied by whole-body autoradiography.

The distribution of [2,3-14C]acrylamide was studied in fingerling rainbow trout by whole-body autoradiography. Fish weighing approximately 7 g were injected ip with 3.2 mg/kg [14C]acrylamide (0.1 microCi/g). One group of fish was kept in a fresh flowing water tank and frozen in dry ice/hexane 22 hr after injection; another group was placed in a separate tank of fresh flowing water and frozen 120 hr after treatment. A third group of fish served as nontreated controls. The autoradiographs of the fish at 22 hr show the highest concentration of radioactivity in the kidney, urinary bladder, blood, gallbladder, intestinal contents, and lens of eye. Lesser amounts of radioactivity are seen in the CNS, liver, and gills. Very low concentrations are seen in muscle. By 120 hr the only high concentrations are seen in gallbladder and lens of the eye. Lesser amounts are seen in the sclera, vertebrae, CNS, kidney, wall of intestine, and discrete spots in subcutaneous tissue presumed to be chromatophores. Low amounts are seen in muscle, the tissue usually consumed by man.

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PubMed1989

Effects of acrylamide and 2,5-hexanedione on brain mitochondrial respiration.

The effects of acrylamide (ACR) and 2,5-hexanedione (2,5-HD) on brain mitochondrial respiration were assessed. Mitochondria were isolated from whole brains or brain regions of control and neurotoxicant-treated rats. Direct in vitro exposure of isolated brain mitochondria to ACR (1 mM final concentration) had no effect on respiration, whereas direct exposure to 2,5-HD (1 mM final concentration) inhibited state 3 respiration. Chronic treatment of rats with ACR (50 mg/kg/day x 10 days) did not affect respiration of mitochondria isolated from cortex or brainstem. However, in mitochondria from cerebellum of ACR treated rats, pyruvate + oxaloacetic acid (pyr/oaa) supported oxygen consumption was decreased significantly in both states 3 and 4. In addition, the ADP/O ratio was reduced in this brain structure. In all brain regions of 2,5-HD (400 mg/kg/day x 24 days) intoxicated rats, pyr/oaa supported state 3 respiration was reduced. Glutamate + malate (glu/mal) supported respiration was diminished only in mitochondria isolated from brain stem of 2,5-HD treated rats. In contrast, the non-neurotoxic analogs, 1,6-hexanediol and N,N'-methylene-bis-acrylamide did not alter mitochondrial respiration in parallel experiments. Thus, both ACR and 2,5-HD produce a substrate-dependent, toxicologically specific inhibition of brain mitochondrial respiration. This inhibition of mitochondrial energy production might play a role in the neurotoxic mechanisms of action for these chemicals.

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PubMed1989

Short-term studies of the effect of acrylamide on the testes of the Egyptian toad.

The treatment of male Egyptian toads (Bufo regularis) with acrylamide (1 mg/toad twice a week for four weeks) was followed by atrophy of the testes, inhibition of spermatogenesis and necrosis of the seminiferous tubules with signs of vacuolation. Ultrastructurally, the Leydig cells of treated toads displayed varying degrees of vacuolation of the mitochondria, with a decrease in the number of ribosomes. The mechanism of the action of acrylamide in inhibiting spermatogenesis may be due to a decrease in the testosterone level, as borne out by vacuolation of the mitochondria and the decrease in the ribosomes in the Leydig cells of treated animals.

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