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  • 1
    Electronic Resource
    Electronic Resource
    Transfer and distribution of accumulated (14C)polychlorinated biphenyls from maternal to fetal and suckling rats (1986)
    Springer
    Archives of environmental contamination and toxicology 15 (1986), S. 709-715 
    Details
    ISSN: 1432-0703
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Medicine
    Notes: Abstract (14C)polychlorinated biphenyls [PCBs (KC-600)] were administered orally to female rats at the dose of 10 mg/kg in olive oil once a week for five weeks. Four weeks after the last administration of (14C)PCBs, they were mated with untreated males. The distribution of total14C was examined in maternal and offspring tissues. The average amount of PCBs accumulated in dams was 44.2% of the dose two weeks after the last administration. The average amount transferred from dam to fetus was 0.003% accumulated in the dam. In the fetus, the highest concentration was found in the fetal placenta followed by the liver, heart, skin, muscle, blood, lung, and brain. The PCBs level in fetal blood was the same as in maternal blood. The average concentration of PCBs in milk was 1.84 ppm. The amount transferred to sucklings increased gradually to about 5% of the maternal PCBs. In suckling rats, PCBs were distributed at the highest concentration in adipose tissues and at intermediate concentrations in the skin, adrenal gland, and liver. The liver to body weight ratio of offspring was significantly increased on the 11th and 25th days after birth. The nursing rats had lower PCBs concentrations compared with the pregnant and virgin rats. The organ concentrations of PCBs in dam and offspring were about ten times as high as those found after treatment with Kane-chlor®-400. These results may suggest that PCBs with higher chlorine content remained in tissues for a longer period of time.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01054917
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  • 2
    Electronic Resource
    Electronic Resource
    Anemia and porphyria caused by N,N′-methylene-bis-acrylamide (MBA) in Mice and rats (1982)
    Springer
    Archives of toxicology 50 (1982), S. 47-55 
    Details
    ISSN: 1432-0738
    Keywords: N,N′-Methylene-bis-acrylamide ; Anemia ; Porphyria ; Mice ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of N,N′-methylene-bis-acrylamide (MBA), a cross-linking agent, on blood and bone marrow after repeated oral doses, were studied in mice and rats. Body weight, three major elements of the blood — erythrocytes, leucocytes and platelets — reticulocytes and bone marrow cells, were all reduced in either or both animals, especially in mice. Phenobarbital (PB) treatment did not greatly modify the effects of MBA in mice. An increase in free erythrocyte porphyrins and a decrease in ALA-D activity were observed in both animals. Urinary porphyrins were elevated in rats after MBA-dosing. PB-treatment did not significantly affect the elevation of porphyrins. After cessation of the MBA-dosing, all these changes were inclined to be restored to normal levels. Amounts of liver total porphyrins and microsomal P-450, and red cell fragility were within normal ranges in mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00569236
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  • 3
    Electronic Resource
    Electronic Resource
    Neurotoxicity of acrylamide and related compounds in rats (1983)
    Springer
    Archives of toxicology 54 (1983), S. 203-213 
    Details
    ISSN: 1432-0738
    Keywords: Acrylamide analogues ; Acrylamide ; N-tert-Butylacrylamide ; Crotonamide ; Diacetone acrylamide ; N-Hydroxymethylacrylamide ; N-Isopropylacrylamide ; Methacrylamide ; N-Methylacrylamide ; Neurotoxicity ; Rotarod performance ; Histopathology ; Neurotubulin ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Neurotoxic properties of acrylamide and seven related compounds in rats were studied with regard to the effects on rotarod performance, morphology of nerves and neurotubulin. Compounds used in the present study were acrylamide, N-hydroxymethylacrylamide, N-isopropylacrylamide, methacrylamide, N-methylacrylamide, crotonamide, diacetone acrylamide, and N-tert-butylacrylamide. Animals were given chemicals in their drinking water for 90 days. Deficit of rotarod performance was produced by five compounds; acrylamide, N-hydroxymethylacrylamide, N-isopropylacrylamide, methacrylamide, and N-methylacrylamide. Morphological changes in tibial and sural nerves, such as shrinkage and loss of myelinated fibres, myelin retraction, and corrugated myelin sheaths, were observed after treatment with these five compounds. Depression of the [3H]colchicinebinding to neurotubulin (the soluble protein) of sciatic nerves was detected after giving these five compounds. After acrylamide dosing, the depression progressed with time. A significant reduction of the colchicine-binding to neurotubulin was also detected in the spinal cord of both the cervical and the lumbar regions, but neither in the brain nor the cerebellum.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01239204
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of N,N′-methylene-bis-acrylamide (MBA) on mouse germ cells — sperm count and morphology, and testicular pathology (1988)
    Springer
    Archives of toxicology 62 (1988), S. 54-59 
    Details
    ISSN: 1432-0738
    Keywords: N,N′-methylene-bis-acrylamide ; Single oral dose ; Sperm count and morphology ; Testicular histopathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The sperm count and morphology, and testicular histopathology were studied in mice over a period of 75 days following a single oral administration of 50, 100, and 200 mg/kg N.N′-methylene-bis-acrylamide (MBA). With a 50 and 100 mg/kg dose, the sperm abnormality reached a maximum at 30 days, whereas the sperm count reached a minimum at 35 days. The abnormality and decrease in sperm count were both dose dependent. Following the administration of 200 mg/kg MBA, the appearance of abnormal sperm showed a diphase pattern, i.e., first at 7–15 days without any reduction of the sperm count and second at 30 days after treatment. Testicular histopathological changes showed that resting spermatocytes, succeeding leptotene and zygotene spermatocytes were either absent or reduced 1–3 days after treatment with 200 mg/kg MBA. These early histopathological changes seemed to precede both the increase in abnormal sperm and the decrease in sperm count observed 30–35 days post-treatment, and also suggested that resting spermatocytes were most sensitive to MBA exposure among various spermatogenic cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00316258
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  • 5
    Electronic Resource
    Electronic Resource
    Neuron and glial cell marker proteins as indicators of heavy metal-induced neurotoxicity in neuroblastoma and glioma cell lines (1993)
    Springer
    Archives of toxicology 67 (1993), S. 491-496 
    Details
    ISSN: 1432-0738
    Keywords: Neurotoxicity ; In vitro test ; Neurospecific marker proteins ; Mercury chloride ; Cadmium chloride
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The sensitive and specific biochemical indicators for assessing chemical-induced neurotoxic insults in cell culture models have not been sufficiently explored. This study was designed to assess the usefulness of glia-specific beta-S100 protein and neuron-specific enolase (NSE) as indices of in vitro neurotoxicity of heavy metals. Glioma C6 and neuroblastoma N18TG-2 cells were grown in Dulbecco's modified Eagle's medium containing various concentrations of mercuric chloride (HgCl2) or cadmium chloride (CdCl2) for 5 days. Toxic response patterns of the neurospecific endpoints (beta-S100 and NSE), which were monitored with enzyme immunoassays, were compared with those of the non-neurospecific endpoints such as cell viability, total cellular protein, lactate dehydrogenase (LDH) activity, and cumulative glucose consumption in the two cell lines. Both HgCl2 and CdCl2 produced dose-dependent inhibition of neurospecific endpoints and non-specific endpoints. However, by ranking the EC50 values (effective concentration producing half-maximal inhibition) for various endpoints, the lowest values were found for beta-S100 in C6 cells, and for NSE in N18TG-2 cells. In lower and intermediate concentrations, the inhibitory effects of the heavy metals on the content of beta-S100 and NSE occurred in the absence of any detectable effect on intracellular LDH activity, and independently of total cellular protein inhibition. The sensitive and excess responses of the neurospecific endpoints relative to that of the non-specific endpoints may reflect the specific neurotoxic insults of the heavy metals on the cultured cells. The highly sensitive and nerve cell-specific changes of the two marker proteins after in vitro treatments with HgCl2 and CdCl2 indicate their usefulness as indicators of in vitro assessment of neurotoxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01969920
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  • 6
    Electronic Resource
    Electronic Resource
    Structure-toxicity relationship of ethylene glycol ethers (1992)
    Springer
    Archives of toxicology 66 (1992), S. 368-371 
    Details
    ISSN: 1432-0738
    Keywords: Ethylene glycol monomethyl ether ; Ethylene glycol monoethyl ether ; Ethylene glycol monoisopropyl ether ; Ethylene glycol monoallyl ether ; Ethylene glycol mono-n-butyl ether ; Ethylene glycol monoisobutyl ether ; Ethylene glycol mono-t-butyl ether ; Ethylene glycol mono-n-hexyl ether ; Ethylene glycol monophenyl ether ; Glioma ; Mouse ; Neuroblastoma ; Structure-toxicity relationship
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The ultimate purpose of the present study was to evaluate correlations between acute in vivo and in vitro toxicity and log P (P is n-octanol-water partition coefficient). The in vitro toxicity to cloned cells (neuroblastoma N18TG-2 and glioma C6) in culture (ED50) and the in vivo toxicity to mice (LD50) of ethylene glycol ethers were studied in terms of the structure-activity relationship. The test ethers showed a wide range of ED50 values in both cells. LD50 was determined under two conditions: LD50-cont. was estimated in mice pretreated with olive oil and LD50-CCl4 in CCl4-pretreated mice. Multiple regression analyses revealed a significant correlation between log 1/LD50 and log P as follows: log (1/LD50−cont.) = − 0.120 (log P)2+0.4871og P−1.182, and log (1/LD50-CCl4) = −0.128 (log P)2+0.5661og P−1.157. There was no significant correlation either between ED50 and LD50 or between ED50 for N18TG-2 and ED50 for C6. The results suggest that metabolic activation might not occur during acute toxicity from the ethers, and that hydrophobicity, expressed as log P, plays an important role in acute toxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01973634
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  • 7
    Electronic Resource
    Electronic Resource
    Neurotoxicity of acrylamide and related compounds and their effects on male gonads in mice (1981)
    Springer
    Archives of toxicology 47 (1981), S. 179-189 
    Details
    ISSN: 1432-0738
    Keywords: Acrylamide analogues ; Acrylamide ; N-tert-Butylacrylamide ; Crotonamide ; Diacetone acrylamide ; N,N-Diethylacrylamide ; N,N-Dimethylacrylamide ; N-Hydroxymethylacrylamide ; Iodoacetamide ; N-Isobutoxymethylacrylamide ; N-Isopropylacrylamide ; Methacrylamide ; N-Methylacrylamide ; N,N′-Methylene-bis-acrylamide ; N-tert-Octylacrylamide ; Neuropathy ; Testicular damage ; Phenobarbital ; Mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Neurotoxicity of acrylamide and related compounds and their effects on the testis after repeated oral doses were studied in mice. Of fourteen analogues tested, five produced neuropathy. In decreasing order of potency as assessed by the rotarod performance test, these were as follows: acrylamide 〉 N-isopropylacrylamide 〉 N-methylacrylamide = methacrylamide 〉 N-hydroxymethylacrylamide. The development of neurotoxicity was either greatly reduced or delayed by phenobarbital treatment. Acrylamide, N-hydroxymethylacrylamide, N-isopropylacrylamide, N-methylacrylamide and N,N′-methylene-bis-acrylamide produced testicular atrophy. Atrophy was either prevented by phenobarbital treatment, as in the cases of acrylamide and N-isopropylacrylamide, or reduced, as in the case of N-hydroxymethylacrylamide. Histological changes in the testis produced by the active compounds were degenerations of the epithelial cells of the seminiferous tubules, with the interstitial cells being normal.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00368678
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  • 8
    Electronic Resource
    Electronic Resource
    Cytotoxicity of acrylamide and related compounds to mouse neuroblastoma and rat Schwannoma cells (1988)
    Springer
    Archives of toxicology 61 (1988), S. 298-305 
    Details
    ISSN: 1432-0738
    Keywords: Acrylamide ; N-Hydroxymethylacrylamide ; Methacrylamide ; N-Isopropylacrylamide ; N-Methylacrylamide ; N,N-Dimethylacrylamide ; Crotonamide ; N,N-Diethylacrylamide ; Diacetone acrylamide ; Dibutyryl cyclic AMP ; Cytotoxicity ; Neuroblastoma ; Schwannoma ; Kinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cytotoxicity of acrylamide and related compounds to mouse neuroblastoma N18TG-2 and rat Schwannoma RT4 cells was studied. Of nine test chemicals, acrylamide and N-hydroxymethylacrylamide were most toxic compared with others on the basis of ED50 value. Observation under phase-contrast microscopy revealed that in N18TG-2 acrylamide produced both degeneration of the cells and inhibition of cell growth, and that in RT4 it produced only inhibition of cell growth without causing any marked morphological changes. Dibutyryl cyclic AMP (dBcAMP) reduced the Cytotoxicity of acrylamide to both types of cells on the basis of the dose-effect curve. Studies on the subcellular distribution of 14C-acrylamide incorporated showed that more than 90% of the total radioactivity was incorporated in the 15000 g supernant fraction. Kinetics of acrylamide uptake by N18TG-2 cells showed that in the cells untreated with dBcAMP there were two binding sites with high and low affinity, and that after treatment with dBcAMP the site of high affinity disappeared. The situation was true for RT4 cells, the results indicating that the immature cells are more vulnerable to acrylamide than the mature cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00364853
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  • 9
    Electronic Resource
    Electronic Resource
    Neurofilament degradation in the nervous system of rats intoxicated with acrylamide, related compounds or 2,5-hexanedione (1988)
    Springer
    Archives of toxicology 62 (1988), S. 70-75 
    Details
    ISSN: 1432-0738
    Keywords: Acrylamide ; N-Hydroxymethylacrylamide ; N-Isopropylacrylamide ; Methacrylamide ; Diacetone acrylamide ; 2,5-Hexanedione ; Axonopathy ; Calcium activated neutral protease ; Neurofilament
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Degradation of neurofilament (NF) proteins by Ca2+-activated neutral protease (CANP) was studied in the nervous system of rats treated with neurotoxic or non-neurotoxic compounds. In the tibial nerve, the degradation of NF 68K was depressed by five neurotoxic compounds: acrylamide, N-hydroxymetylacrylamide, N-isopropylacrylamide, methacrylamide and 2,5-hexanedione. A non-neurotoxic compound, diacetone acrylamide, did not show any effect on the degradation. An immunoblot analysis confirmed the reduction in the degradation and revealed a difference in the degradation pattern between the control and acrylamide-treated rats. In the spinal cord, the degradation of the three subunits of NF was depressed in animals treated with acrylamide. Although the exact mechanism of the reduction in the degradation of NF is not yet known, the present results suggest that an inhibitory effect on CANP activity might be relevant to the mechanism of neurotoxic action of acrylamide derivatives.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00316261
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  • 10
    Electronic Resource
    Electronic Resource
    Studies on the mechanism of acute toxicity of nitriles in mice (1984)
    Springer
    Archives of toxicology 55 (1984), S. 47-54 
    Details
    ISSN: 1432-0738
    Keywords: Mononitriles ; Acetonitrile ; Propionitrile ; 3-Hydroxypropionitrile ; 3-Chloropropionitrile ; Acrylonitrile ; Methacrylonitrile ; n-Butyronitrile ; Isobutyronitrile ; Allylnitrile ; 4-Chlorobutyronitrile ; 2-Methylbutyronitrile ; Phenylacetonitrile ; 3-Phenylpropionitrile ; Chloroacetonitrile ; n-Valeronitrile ; Isovaleronitrile ; n-Capronitrile ; Isocapronitrile ; Caprylonitrile ; Pelargononitrile ; Benzonitrile ; Carbon tetrachloride ; Structure toxicity relationship ; Metabolism ; Mouse hepatic microsomal enzymes ; Cyanide ion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Acute toxicity and metabolism of 21 nitriles in mice were studied in relation to their chemical structures. All the test nitriles liberated cyanide ions both in vivo and in vitro, with the exception of benzonitrile, although the extent of liberation and the effect of carbon tetrachloride (CCl4) pretreatment on the mortality of animals differed among nitriles. From these results, test compounds were tentatively divided into three groups. In group 1 (13 compounds), acute toxicity was greatly reduced by CCl4 pretreatment, in group 2 (seven compounds), toxicity was not significantly changed or was somewhat enhanced, and in group 3, benzonitrile only, toxicity was clearly enhanced. The amount of cyanide was higher (0.68–0.80 μg CN/g brain) at death in the brains of mice given group-1 compounds, the level being comparable to that found in mice killed by dosing with potassium cyanide. After oral doses of each nitrile, the time course for cyanide levels in the liver varied among the compounds. The difference between group-1 and -2 compounds lay in the dose-cyanide liberation relationship in liver, and in the kinetics for cyanide liberation in the hepatic microsomal enzyme system. Double-reciprocal plots of enzyme activity showed a linear relationship for nitriles of group 1 and a non-linear one for group 2. The relationship between log (1/LD50) and log P for the compounds in group 1 fitted a parabolic plot, while that for compounds in group 2 was linear.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00316585
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