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PubMed1992

Brain energy metabolites in mice intoxicated with acrylamide: effects of ischemia.

Concentrations of phosphocreatine, creatine, ATP, ADP, AMP, glucose and lactate in the whole brain did not differ between the mice intoxicated with acrylamide and the controls. When the brain was made ischemic, these concentrations changed to the same extent in both groups. The only difference was the lower pyruvate in acrylamide-intoxicated mice under the ischemia. Thus, as far as the whole brain is concerned, acrylamide does not cause gross alterations of energy metabolites, even under ischemia.

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PubMed1993

Determination of acrylamide in rat serum and sciatic nerve by gas chromatography-electron-capture detection.

A modified method for the derivatization and determination of acrylamide as 2-bromopropenamide by gas chromatography-electron-capture detection was developed and applied to serum and sciatic nerve from rats. The method was accurate and precise over the calibration range 2.24-7.47 micrograms/ml in serum diluted 1:125 and 4-122 micrograms/g in sciatic nerve homogenate (5 mg/ml). limits of detection were estimated to be 1200 ng/ml in undiluted serum and 3 micrograms/g in intact sciatic nerve. The use of less dilute samples to allow for lower limits of detection appears feasible. The time-course of acrylamide in serum and sciatic nerve was studied after acute dosing and indicated elimination half-lives of 1.8 and 2.0 h for serum and sciatic nerve, respectively. A dose-effect relationship was established for each matrix after acute dosing and the measured acrylamide concentrations in serum (microgram/ml) were approximately the same as in sciatic nerve (microgram/g).

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PubMed1998

Time-resolved and steady-state fluorescence quenching of N-acetyl-L-tryptophanamide by acrylamide and iodide.

We examined the time-resolved and steady-state fluorescence quenching of N-acetyl-L-tryptophanamide (NATA) by acrylamide and iodide, over a range of viscosities in propylene glycol. The quenching of NATA by acrylamide and iodide results in heterogeneity of the intensity decay which increases with the quencher concentration. We attribute the complex decays of NATA to transient effects in diffusion and the nature of the fluorophore-quencher interaction. These data were compared using the phenomenological radiation boundary condition (RBC) and distance-dependent quenching (DDQ) models for collisional quenching. We used global analysis of the time-resolved frequency-domain and steady-state data to select between the models. Consideration of both the frequency-domain and steady state data demonstrate that the quenching rate depends exponentially on the fluorophore-quencher distance, indicating the validity of the DDQ model. The rate constants for acrylamide and iodide quenching, at the constant distance of 5 A, were found to be near 10(13) s-1 and 10(9) s-1, respectively. These rates reflect electron transfer and exchange interactions as the probable quenching mechanisms, respectively.

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PubMed1997

Somatic and germ cell mutagenesis in lambda lacZ transgenic mice treated with acrylamide or ethylnitrosourea.

The transgenic Muta Mouse in vivo mutagenesis assay was employed to determine the activity of acrylamide and ethylnitrosourea in liver and germ cells after 3, 10 and 100 days following treatment. Each cell of the Muta Mouse carries 80 copies of the lambda gt10 phage including the bacterial lacZ gene, which act as the target gene for the mutagenesis assay. Groups of Muta Mice were given a single intraperitoneal injection of 80 or 160 mg/kg ethylnitrosourea or 50 or 100 mg/kg acrylamide. The tissues were prepared 3, 10 or 100 days post treatment. The liver genomic DNA was extracted with the manufacturer's standard protocol, while the genomic germ cell DNA was extracted with 4 different methods due to problems encountered in DNA yields and packaging efficiency. The mutation analysis of the lacZ gene was carried out by the positive selective assay method [Gossen et al. (1989) Proc. Natl. Acad. Sci. USA, 86, 7971-7975; Dean and Myhr (1994) Mutagenesis, 9, 183-185]. There was a slight increase due to treatment of the observed mutation frequencies in the acrylamide liver group for all three assay times. From the day 3 group to the day 100 group a time dependent decrease in all the absolute mutant frequencies was detectable. The ethylnitrosourea liver group showed a time- and dose-dependent increase in the mutant frequencies from day 3 to day 100. No meaningful results were obtained for the germ cell tissue assays due to the low amount of genomic DNA extracted which was not packageable in the lambda lacZ assay. At present for the mutagenesis assay of isolated spermatozoa in our laboratory we would be forced to pool tissues from animals to obtain enough DNA for an assay. Since 'jackpot'-animals may exist [Heddle et al. (1992) Mutation Res., 272, 195-203] the individual animals of such a pooled analysis group must be tested before pooling.

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PubMedDate not supplied

2,5-Hexanedione and acrylamide produce reorganization of motoneuron perikarya.

During acrylamide and hexacarbon exposure few changes have been reported in motoneuron perikarya. In the present study, light microscopic examination of lumbar motoneurons from rats intoxicated with either 2,5-hexanedione (2,5-HD) or acrylamide showed relatively few nonspecific changes compared to controls. However, ultrastructural study of 2,5-HD-intoxicated perikarya revealed a range of cytological reorganization: nuclear eccentricity and capping, reduced numbers of large Nissl bodies, and mitochondrial hypertrophy and hyperplasia. In 2,5-HD-intoxicated perikarya, computer-assisted stereologic analysis demonstrated a significant increase in the volume density of mitochondria. Ultrastructurally, acrylamide-intoxicated perikarya showed a marked reduction in the size of Nissl bodies. Stereologic analysis showed reductions in Nissl bodies, granular endoplasmic reticulum and Golgi complexes, and an increase in mitochondria. Taken together, these qualitative and morphometric changes, which were not obvious on light microscopic examination, imply significant reorganization of perikaryal metabolism.

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PubMed1984

Abnormalities of oesophageal mechanoreceptors in canine acrylamide neuropathy.

Dogs exposed to acrylamide develop peripheral neuropathy and megaoesophagus. The properties of slowly adapting oesophageal mechanoreceptors were studied in six control and five acrylamide affected greyhounds in which the oesophagus had been surgically isolated under anaesthesia and oesophageal pressure was controlled while monitoring impulses in oesophageal afferent fibres in the cervical vagus. In the acrylamide affected animals oesophageal afferent units had elevated thresholds and significantly reduced firing rates during ramp increases in oesophageal pressure. It is concluded that abnormalities of oesophageal mechanoreceptors may be important in the pathogenesis of certain oesophageal motility disorders in man and animals.

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PubMed1986

Abnormal pulmonary slowly adapting receptors in canine acrylamide neuropathy.

Slowly adapting lung stretch receptors (SARs) and their vagal afferents are considered to play an important role in the mediation of numerous respiratory reflexes. The understanding of such reflexes has been facilitated by altering the discharge properties of SARs or by preventing the conduction of SAR-generated impulses to the brain stem. In a number of naturally occurring diseases of the peripheral nervous system, the vagus nerve and vagal reflexes are damaged. We have studied the function of SARs in anesthetized dogs with acrylamide neuropathy, a distal axonopathy that has been used as a model of naturally occurring neuropathies. There was a marked increase in threshold and decrease in firing rate of SARs in dogs with moderate neuropathy. Abnormal SAR discharge patterns were observed, and there was a depletion of those units innervated by the fastest conducting vagal afferent fibers in treated animals. Acrylamide induced degeneration of myelinated fibers in bronchial branches of the vagus nerve. These abnormalities were partially reversed upon withdrawal of the neurotoxin. Acrylamide may be a useful agent in the study of vagally mediated respiratory reflexes. SAR function is likely to be abnormal in diseases of the peripheral nervous system.

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PubMed1986

Comparison of central and peripheral nervous system lesions caused by high-dose short-term and low-dose subchronic acrylamide treatment in rats.

The effects of high-dose subacute acrylamide treatment of up to 50 mg/kg/day for 4 or 10 d were compared to those of subchronic exposure, up to 12 mg/kg/day for 90 d. In the subacute study, Purkinje cells, long ascending tracts of the spinal cord, optic tract terminal or preterminal regions in superior colliculus, sensory ganglion cells, and distal large-caliber peripheral axons were severely affected. Purkinje cells and fasciculus gracilis changes were the earliest lesions. In the subchronic study, the dominant lesion was confined to the distal peripheral axon, with only minor changes occurring in spinal cord and medulla. Paranodal swellings with the characteristic appearance of neurofilament aggregations were not seen. This morphological study suggests a significant difference between high- and low-dose acrylamide-induced lesions. If there is a reduced tendency for long-term low-dose acrylamide exposure to produce CNS lesions, the risk of irreversible nervous system damage would be less than that predicted from subacute studies.

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PubMed1988

Acrylamide and iodide fluorescence quenching studies on whole human lenses and their protein extracts.

Tryptophan fluorescence was monitored in whole lenses (and in soluble crystallin fractions derived from these lenses) before and after incubating them in media containing acrylamide or iodide. The effects of exposing one lens to low level broadband UV radiation were compared with the contralateral lens incubated in the dark. In addition we employed 13C labeled acrylamide in order to monitor (by NMR spectroscopy) which crystallins were most effected. These studies demonstrate an acrylamide fluorescence quenching effect in whole lenses and extracted lens proteins, which is directly age related, as is the extent of its incorporation and binding to specific lens proteins. Iodide had no effect on TRP fluorescence in whole lenses and a slight effect on the extracted crystallins. These data demonstrate differences in the microenvironment of TRP residues in the various lens crystallins and their relative susceptibility to low level UV radiation exposure at doses approaching the ambient in vivo levels in a "real life" situation. This approach helps to delineate the microenvironment of TRP residues in native proteins and the effects of UV exposure on proteins with buried versus exposed TRP residues.

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PubMed1992

["Toxins" and nerve--a discussion on the pathogenesis of acrylamide intoxication, giant axonal neuropathy and Krabbe disease].

A common mechanism appears to play a pathogenetic role in acrylamide intoxication, which is due to an exogenous cause, and in giant axonal neuropathy, an intrinsic disorder. In giant axonal neuropathy, a genetic defect in the processing of an intrinsic acrylamide or acrylamide-like substance may be postulated. On the other hand, the devastating pathology in Krabbe disease (a genetic disorder affecting almost exclusively the nervous system) appears to be due to the effects of psychosine, a toxic lipid produced in the nervous system. These suggest that the "toxicological approach" can be more diverse and of greater use than usually considered.

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PubMed1992

Comparative studies on the neuro- and reproductive toxicity of acrylamide and its epoxide metabolite glycidamide in the rat.

The neurotoxicity of acrylamide (AA) has been the subject of extensive studies at the morphological and functional levels in both animals and man. The concern for human exposure to monomeric AA derives partly from its extensive use in molecular biology laboratories where, in the United States alone, 100,000-200,000 persons are potentially exposed. Initial work in this laboratory aiming at the development of techniques for using hemoglobin adducts as biomarkers for human exposure to AA, revealed the formation of glycidamide as a reactive epoxide metabolite of acrylamide in the rat (Chem. Res. Toxicol. 3, 406, 1990). In rats treated with 0-100 mg/kg of AA significant dose-rate effects were observed on adduct formation by both AA and glycidamide. The high rate of formation of the metabolite, especially at low doses where approximately 60% of AA was converted to glycidamide in vivo, prompted us to investigate its potential role in the induction of neurotoxic and reproductive effects attributed to AA exposure. In initial neurotoxicological experiments, the effects of the parent compound (8-14 days, 25 and 50 mg/kg/day) and the metabolite (8-14 days, 50 and 100 mg/kg/day) were compared. While at the higher dose both compounds affected the rats' performance on the rotarod, only acrylamide had a significant effect in the hindlimb splay test, which is considered a more sensitive indicator of peripheral neuropathy. On the other hand, a stronger effect was seen for glycidamide than for AA on the male reproductive system, especially on sperm cell viability.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1992

Acrylamide: dermal exposure produces genetic damage in male mouse germ cells.

Acrylamide is used extensively in sewage and wastewater treatment plants, in the paper and pulp industry, in treatment of potable water, and in research laboratories for chromatography, electrophoresis, and electron microscopy. Dermal contact is a major route of human exposure. It has been shown that acrylamide is highly effective in breaking chromosomes of germ cells of male mice and rats when administered intraperitoneally or orally, resulting both in the early death of conceptuses and in the transmission of reciprocal translocations to live-born progeny. It is now reported that acrylamide is absorbed through the skin of male mice, reaches the germ cells, and induces chromosomal damage. The magnitude of genetic damage appears to be proportional to the dose administered topically.

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PubMed1991

Gene probe for P0 messenger RNA used to index acrylamide toxic neuropathy in rats.

Cumulative exposure to the neurotoxicant acrylamide produces axonal damage in the distal ends of both central (CNS) and peripheral (PNS) nerve fibers and subsequent hind-limb paralysis. The messenger RNA which codes for the PNS myelin glycoprotein P0 (P0-mRNA) was used to monitor this toxic neuropathy in Sprague Dawley rats prior to, concurrent with, and subsequent to, ultrastructurally and immunocytochemically defined nerve damage. Rats were dosed every other day with acrylamide (50 mg/kg, IP) and sampled intermittently throughout a 4 week exposure period. Slot blot and Northern gel analyses of the proximal and distal sciatic nerve were used to determine a quantitated measure of P0-mRNA. Twenty-four hours after the first treatment, in the absence of ultrastructural damage, P0-mRNA increased 55% over control levels in the distal sciatic nerve. After 12 treatments, and concomitant with the appearance of spinal cord and PNS neuropathic damage and hindlimb dysfunction, P0-mRNA decreased 45% below control levels. Levels of P0-mRNA from rats exposed to 12 treatments of acrylamide but allowed to recover for 40 days, returned to 79% of control values to reflect the regeneration and remyelination occurring in the distal sciatic nerve. In spite of these fluctuations in levels of P0-mRNA, immunocytochemical staining of P0 protein in plastic sections of the distal sciatic nerve was present throughout all sample times. These results suggest that changes in neural specific mRNAs are sensitive to neurotoxic damage and can be used to monitor the pathogenesis of nerve degeneration.

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PubMed1990

Analysis of dose/time/response relationships for chronic toxic effects: the case of acrylamide.

This case study illustrates how a very simple dynamic modeling approach can extract information of interest for both toxic mechanism research and risk assessment from a series of dose/time/response data. The technique is applicable for effects that are thought to result from damage processes that are reversible, at least at low doses and times of exposure. The data sets analyzed provided information on some specific manifestation of acrylamide neurotoxicity produced by different combinations of acrylamide dose rate and duration of exposure. Assuming that responses occur when a specific amount of axonal damage accumulates, and that the repair of damage depends directly on the amount of damage present, the dose-related change in the time required to produce a specific type of effect can be used to estimate: (1) The rate of repair of the incipient damage - and differences in repair rates for different individuals within species, and among different species, and (2) The dose of acrylamide that would be just barely able to produce each effect in each species, if the experiment were conducted over the animal's entire lifespan. Information of the first type may also be helpful in neurotoxicology research. Specific biomarkers for the main process causing a particular response should be repaired in different locations and in different species with the dynamics that are consistent with the repair rates calculated from the dose vs. time-of-effect data.

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PubMed1986

Separation of apolipoprotein B species by agarose-acrylamide gel electrophoresis.

Human apolipoprotein (apo) B has been recognized to exist in two different forms designated apoB-100 and apoB-48. The two apoB forms are usually separated by NaDodSO4 gel electrophoresis with a low percentage polyacrylamide gel in a tube gel apparatus. However, the matrix of this low percentage gel is relatively weak, and one can separate the two forms of apoB in a slab gel apparatus only if one utilizes a gradient polyacrylamide gel or a higher percentage polyacrylamide gel which results in a poorer separation of the protein bands. We have developed an agarose-acrylamide gel electrophoretic method to separate the two major apoB forms. The gel is a mixture of 0.5% agarose and 2% acrylamide. The agarose-acrylamide method is fast, has the advantage of being able to be used on an analytical or preparative scale in a vertical slab gel apparatus, and the gel is of sufficient strength to be used in immunoblotting and/or radioautography.

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PubMed1985

Acrylamide effects on the macaque visual system. I. Psychophysics and electrophysiology.

Oral acrylamide produces axonal swelling and later degeneration and gliosis in the distal optic tract, especially within the lateral geniculate nucleus, of macaque monkeys. Measures of visual thresholds and cortical-evoked potentials were used to study the time course of visual changes during exposure to acrylamide in macaque monkeys. Contrast sensitivity, visual acuity, and flicker fusion frequency were reduced during exposure, and only flicker fusion recovered rapidly and completely after exposure. Pattern-reversal-evoked responses exhibited increased latency and reduced amplitude during dosing but substantially recovered after exposure. Visual acuity and contrast sensitivity for high spatial frequencies were decreased throughout the 140 days of testing after dosing. These results suggest an acute general depression of visual capacities as the initial effect of acrylamide exposure, whereas later effects were confined to high spatial frequencies.

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PubMed1985

Acrylamide effects on the macaque visual system. II. Retinogeniculate morphology.

Oral acrylamide dosing for 6-10 weeks produced axonal swellings with neurofilament accumulation in the distal optic tract and lateral geniculate nucleus of macaques. No swellings were seen in the retina or optic nerve. Monkeys that were killed 6-8 months after similar dosing showed a marked neuronal degeneration in the visual pathways that was more pronounced after two than after a single period of exposure. This degeneration was characterized by the following: loss of ganglion cells in central retina with relative sparing of other retinal neurons; disproportionate degeneration of temporal to central optic nerve and the dorsal optic tract; and neuronal atrophy in parvocellular layers of the lateral geniculate nucleus, with relative sparing of magnocellular layers. The pattern of neuronal loss suggests that one type of retinal ganglion cell or its axon may be especially vulnerable to damage by acrylamide. The selective neuronal damage produced by acrylamide may help explain the nature of the visual dysfunction associated with this intoxication.

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PubMed1981

Group Ia primary afferent terminal defect in cats with acrylamide neuropathy.

Group la primary afferent terminal (PAT) function was assessed in cats with acrylamide neuropathy. Spinal monosynaptic input-output relationships, critical input, the ability to maintain repetitive discharge at low frequencies, and apparent transmitter turnover parameters were determined in animals with subthreshold, moderate and severe degrees of acrylamide neuropathy (75, 150, and 300 mg/kg, respectively. The monosynaptic pathways of the soleus and medial gastrocnemius motoneuron pools were elicited by stimulation of their respective muscle nerves. The threshold for activation of the monosynaptic reflex (MSR) evoked by both SOL and MG nerves was increased 50% (critical input), regardless of dose regimen. Repetitive stimulation of the MSR at low frequencies (2-10 Hz) produces a slow decline in amplitude until it reaches a plateau. The height of the plateau attained in neuropathic cats was considerably lower than the controls. Determination of apparent transmitter turnover parameters in neuropathic cats showed that the constant fraction of neurotransmitter released from group la PAT remained the same while the rate of replenishment of transmitter available for release was attenuated in both SOL-VR and MG-VR pathways. The increase in the critical input and decrease in the rate of replenishment points up a functional defect in a group la PAT in cats with acrylamide neuropathy.

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