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  • 1
    Electronic Resource
    Electronic Resource
    Alkylation of RNA by vinyl bromide metabolites in vitro and in vivo (1979)
    Springer
    Archives of toxicology 41 (1979), S. 279-286 
    Details
    ISSN: 1432-0738
    Keywords: Vinyl bromide ; RNA alkylation ; 1,N6-ethenoadenosine ; 3,N4-ethenocytidine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract [1,2-14C]Vinyl bromide was incubated with rat liver microsomes, NADPH, and polyadenylic acid, polycytidylic acid, or RNA, respectively. Part of the adenosine moieties in RNA or in polyadenylic acid were alkylated and labelled 1,N6-ethenoadenosine structures were formed. Part of the cytidine moieties were converted into 3,N4-ethenocytidine. In addition, a further unidentified cytidine alkylation product was observed which was not seen in experiments using [1,2-14C]vinyl chloride. When rats were exposed to [1,2-14C]vinyl bromide, radioactive ethenoadenosine and ethenocytidine were present in hydrolysates of liver RNA. A further alkylation product was observed in the RNA hydrolysates which did not occur in experiments using [14C]vinyl chloride. The data show that vinyl bromide metabolites alkylate nucleic acids; although in general in this respect vinyl bromide and vinyl chloride behave similarly, some differences are observed in the alkylation behaviour of both compounds.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296897
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  • 2
    Electronic Resource
    Electronic Resource
    Inhalation pharmacokinetics based on gas uptake studies (1981)
    Springer
    Archives of toxicology 47 (1981), S. 293-304 
    Details
    ISSN: 1432-0738
    Keywords: Acetone ; Pharmacokinetics ; Formate excretion ; Gas uptake
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Inhalation pharmacokinetics of acetone in rats was studied using gas uptake techniques. Under conditions of negligible metabolism (saturation of metabolizing enzymes) the coefficient of distribution K eq between organism and gas phase was 220 which confirmed that acetone is mainly (but not exclusively) distributed within the body water compartment. The metabolic elimination of acetone from the animals followed strict Michaelis-Menten saturation kinetics; the K m corresponded to 160 ppm in the atmosphere, v max was 230 μmol · h−1 · kg−1. A shift in the distribution pattern of acetone under conditions of prevalent metabolism was theoretically predicted and experimentally proven; as the partial process of metabolic elimination was dose-dependent, this “depleted” the animal compartment from acetone in a dose-dependent fashion causing a shift in the “steady-state-constant”, K st . Part of the acetone which was metabolically eliminated (4.7%) appeared in the urine as formate within 7 days after ending a 48-h exposure to acetone; this excretion was linear with time. The data suggested existence of a formate pool in the organism from which formate was released with delay. Hence, limitations may be inferred as to the applicability of urinary formate excretion as a quantitative indicator for changing conditions of acetone exposure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00332395
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  • 3
    Electronic Resource
    Electronic Resource
    Inhalation pharmacokinetics based on gas uptake studies (1984)
    Springer
    Archives of toxicology 55 (1984), S. 219-223 
    Details
    ISSN: 1432-0738
    Keywords: Ethylene ; Ethylene oxide ; 1,3-Butadiene ; Butadiene monoxide (Vinyl oxirane) ; Pharmacokinetics ; Risk assessment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract When ethylene oxide or butadiene monoxide is added to the atmosphere of a closed inhalation chamber occupied by Sprague-Dawley rats, a first-order elimination pattern is observed. When either of these compounds is IP injected into rats which are subsequently placed in the closed chamber, the course of epoxide in the atmosphere follows Bateman exponential functions. From the experimental data, the kinetic parameters for distribution and metabolic elimination of ethylene oxide and butadiene monoxide can be derived. When ethylene or 1,3-butadiene was added to the closed exposure systems and kept at atmospheric concentrations which assured maximal metabolic turnover of the olefin (i.e., concentrations above 1,000 ppm ethylene or 1,500 ppm 1,3-butadiene), exhalation of the appropriate epoxide occurred and led finally to a constant (plateau) concentration of the reactive metabolite in the system's atmosphere. Although the initial time-course was different between butadiene monoxide and ethylene oxide (with a high initial increase of ethylene oxide and a subsequent decrease) an analysis at steady-state (plateau concentrations) revealed that only 29% of the amounts of both epoxides which in theory are formed as primary metabolites from the parent olefins are systematically available (i.e., distributed in the entire organism). The discrepancy is probably related to first pass elimination of the epoxide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00341014
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  • 4
    Electronic Resource
    Electronic Resource
    Fast uptake kinetics in vitro of 51Cr (VI) by red blood cells of man and rat (1985)
    Springer
    Archives of toxicology 57 (1985), S. 31-34 
    Details
    ISSN: 1432-0738
    Keywords: Chromium (III) ; Chromium (VI) ; Kinetics ; Red blood cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Fast transport kinetics of 51Cr (VI) into red blood cells (RBCs) in vitro were studied. No significant species differences were found between RBCs of man and rat. The uptake of 51Cr (VI) by RBCs in whole blood was composed of two different first order processes of different velocities (apparent t1/2 of 22.7 s and 10.4 min for man and 6.9 s and 10.1 min for rat, respectively). However, even after longer time periods a fixed portion of approximately 15% of the administered dose remained in the plasma and did not penetrate into RBCs Over the entire concentration range studied (10 μM–50 mM), the fast initial uptake followed Michaelis-Menten kinetics. The maximal capacity of this Cr(VI) transport into RBCs of man and rat was 3.1×108 CrO4 2− ions × cell−1 × min−1 and 2.5×108 CrO4 −2 ions × cell−1 × min−1, respectively. It is likely that Cr(VI) is transported into RBCs via a physiological anion carrier (“band-3-protein”).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00286571
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  • 5
    Electronic Resource
    Electronic Resource
    Inhalation pharmacokinetics of 1,2-epoxybutene-3 reveal species differences between rats and mice sensitive to butadiene-induced carcinogenesis (1987)
    Springer
    Archives of toxicology 61 (1987), S. 7-11 
    Details
    ISSN: 1432-0738
    Keywords: Butadiene ; Epoxybutene ; Inhalation ; Species differences ; Metabolism ; Pharmacokinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Comparative investigations of inhalation pharmacokinetics of 1,2-epoxybutene-3 (vinyl oxirane, the primary reactive intermediate of butadiene) revealed major differences in metabolism of this compound between rats and mice. Whereas in rats no indication of saturation kinetics of epoxybutene metabolism could be observed up to exposure concentrations of 5000 ppm, in mice saturation of epoxybutene metabolism becomes apparent at atmospheric concentrations of about 500 ppm. The estimated maximal metabolic rate (Vmax) in mice for epoxybutene was only 350 μmol×h−1×kg−1 (rats: 〉2600 μmol× h−1×kg−1). In the lower concentration range where first order metabolism applies (up to about 500 ppm) epoxybutene is metabolized by mice at higher rates compared to rats (metabolic clearance per kg body weight, mice: 24900 ml×h−1, rats: 13400 ml×h−1). Under these conditions the steady state concentration of epoxybutene in the mouse is about 10 times that in the rat. When mice are exposed to high concentrations of butadiene (〉2000 ppm; conditions of saturation of butadiene metabolism; closed exposure system) epoxybutene is exhaled by the animals, and its concentration in the gas phase increases with exposure time. At about 10 ppm epoxybutene signs of acute toxicity are observed. When rats are exposed to butadiene under similar conditions, the epoxybutene concentration reaches a plateau at about 4 ppm. Under these conditions hepatic non-protein sulfhydryl compounds are virtually depleted in mice but not in rats. We conclude that in addition to the higher rate of metabolism of butadiene in mice, limited detoxification and consequently accumulation of its primary reactive intermediate epoxybutene may be a major determinant for the higher susceptibility of mice to butadiene-induced carcinogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00324541
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  • 6
    Electronic Resource
    Electronic Resource
    Preexistence of chronic tubular damage in cases of renal cell cancer after long and high exposure to trichloroethylene (1996)
    Springer
    Archives of toxicology 70 (1996), S. 259-260 
    Details
    ISSN: 1432-0738
    Keywords: Key words Trichloroethylene ; Renal cell cancer ; Tubular damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Substantially more cases of tubular damage were found among renal cell carcinoma patients who had been exposed to high levels of trichloroethylene over many years than among renal cell carcinoma patients who had not been exposed to trichloroethylene. This supports the hypothesis (Goeptar et al. 1995) that chronic tubular damage may be regarded as a necessary precondition for trichloroethylene to exert a nephrocarcinogenic effect. The findings also indicate that the urine protein patterns identified with SDS-PAGE may represent a valuable parameter for effect biomonitoring of persons exposed to high levels of trichloroethylene over many years.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050271
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  • 7
    Electronic Resource
    Electronic Resource
    Evaluation of DNA damage by alkaline elution technique after inhalation exposure of rats and mice to 1,3-butadiene (1993)
    Springer
    Archives of toxicology 67 (1993), S. 34-38 
    Details
    ISSN: 1432-0738
    Keywords: Alkaline elution ; 1,3-Butadiene ; Lung ; Liver ; Mouse ; Rat ; Single-strand breaks ; DNA-DNA cross-links ; DNA-protein cross-links
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The alkaline filter elution technique was used to evaluate single strand breaks (SSB), DNA-DNA (DDCL) and DNA-protein cross-links (DPCL) in liver and lung of male rats (Sprague-Dawley) and male mice (B6C3F1) after exposure to 2000 ppm 1,3-butadiene (BD) for 7 days (7 h/day and/or to 100, 250, 500, 1000) 2000 ppm BD for 7 h. SSB were detected in liver DNA of both species at 2000 ppm. Cross-links are more pronounced in mouse lung than in mouse liver. Elution rates of lung DNA from mice exposed for 7 h to different concentrations of BD revealed an increase in cross-links between 250 and 500 ppm, and a further increase in cross-links up to 2000 ppm. No such signs of genotoxicity could be observed for the lung of rats. Our data support the involvement of reactive metabolites (epoxybutene and especially diepoxybutane) in butadieneinduced carcinogenesis in the mouse but not to that extent in the rat.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02072032
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  • 8
    Electronic Resource
    Electronic Resource
    Dose-DNA adduct relationship for ethylene oxide (1993)
    Springer
    Archives of toxicology 67 (1993), S. 712-713 
    Details
    ISSN: 1432-0738
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01973696
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  • 9
    Electronic Resource
    Electronic Resource
    Glutathione-S-transferase (GST) theta polymorphism influences background SCE rate (1995)
    Springer
    Archives of toxicology 69 (1995), S. 505-507 
    Details
    ISSN: 1432-0738
    Keywords: Key words Glutathione-S-transferase ; Theta polymorphism ; Sister chromatid exchange
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Polymorphism of glutathione S-transferase θ (GSTT1) modulates the toxicity of halogenated alkanes and epoxides in humans. The enzymatic activity of glutathione S-transferase θ and its corresponding gene is lacking in about 30% of the central European population. It has now been demonstrated that the background rate for sister chromatid exchange (SCE) is affected by this particular polymorphism. Smoking as a known inducer of SCE was taken into account. A group of GSTT1-positive subjects exhibited lower SCE rates than GSTT1-negative individuals (7.55±0.77 versus 8.74±1.24 SCE/mitosis, respectively, p〈0.005). Non-smoking GSTT1-positive individuals showed the lowest SCE rate (7.26±0.71 SCE/mitosis), significantly lower than the rates of smoking GSTT1-positive and non-smoking GSTT1-negative subjects (8.14±0.55 SCE/mitosis and 8.12±0.88 SCE/mitosis, respectively, p〈0.025 in both cases). Smoking GSTT1-negative subjects exhibited the highest SCE rates (9.28±1.3 SCE/mitosis). It is hypothesized that GSTT1 is protective against background genotoxic damage. Since ethylene oxide is a proven substrate of GSTT1, the detoxification of this epoxide arising from endogenous ethylene may modulate SCE background rates.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050205
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  • 10
    Electronic Resource
    Electronic Resource
    Increased acetone exhalation induced by metabolites of halogenated C1 and C2 compounds (1982)
    Springer
    Archives of toxicology 49 (1982), S. 107-116 
    Details
    ISSN: 1432-0738
    Keywords: Acetone production ; Halomethanes ; Haloethanes ; Haloethylenes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rats were exposed, in a closed desiccator jar chamber, to concentrations of various halogenated C1 and C2 compounds at which the metabolizing capacities were saturated (V max conditions). Within the exposure period of 50 h concentrations of the xenobiotic and of exhaled acetone were monitored in the gas phase of the system. The quantitative extent of acetone exhalation was dependent on the individual compound examined. Acetone exhalation was stimulated in presence of vinyl chloride, vinyl bromide, vinyl fluoride, vinylidene fluoride, cis-and trans-1,2-di-chloroethylene, trichloroethylene, perchloroethylene, methylene chloride, chloroform, carbon tetrachloride and 1,1,2-trichloroethane. No stimulation of acetone exhalation occured with 1,1,1-trichloroethane and with the reference hydrocarbon n-hexane. Also, acetone exhalation was evoked by infusions of either fluoroacetate or chloroacetate, two anticipated or proven metabolites of some haloethylenes; the infusion rates of which were based on calculations of the metabolic rates of vinylidene fluoride and of vinyl chloride, respectively.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00332358
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