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  • 1
    Electronic Resource
    Electronic Resource
    Effect of dithiocarb and dimethyl sulfoxide on irreversible binding of 14C-bromobenzene to rat liver microsomal protein (1979)
    Springer
    Archives of toxicology 42 (1979), S. 289-293 
    Details
    ISSN: 1432-0738
    Keywords: Bromobenzene ; Diethyl dithiocarbamate ; Dimethyl sulfoxide ; Irreversible binding ; Rat liver microsomes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The irreversible binding of [14C]-bromobenzene to rat liver microsomal protein in vitro was inhibited by dithiocarb and DMSO. Dithiocarb suppressed this binding in a time- and concentration-dependent manner (I50 = 4.5 10−5 M). DMSO reduced the degree of covalent binding by 61% from 5 x 10−5 M to 8 × 10−4 M. Dithiocarb was also effective in inhibiting irreversible binding of bromobenzene to liver protein in vivo. Our results are consistent with the hypothesis that dithiocarb exerts its antihepatotoxic efficacy by depressing microsomal mixed-function oxidase activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00334843
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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
    Long-term effects of commercial and congeneric polychlorinated biphenyls on ethane production and malondialdehyde levels, indicators of in vivo lipid peroxidation (1988)
    Springer
    Archives of toxicology 62 (1988), S. 369-374 
    Details
    ISSN: 1432-0738
    Keywords: Lipid peroxidation ; Malondialdehyde ; Ethane ; Glutathione ; Polychlorinated biphenyls
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Ethane exhalation was increased in male Sprague-Dawley rats following a single intraperitoneal (IP) injection of Aroclor 1254 (500 mg/kg). In the first 2 weeks following Aroclor 1254 treatment, the increase in ethane exhalation was due to an inhibition of metabolism of endogenous ethane rather than to an increase in ethane production. In weeks 3 and 4 following Aroclor 1254 administration, metabolic clearance of ethane returned to and exceeded control levels, while ethane production increased to approximately twice the control rates (day 30). The HPLC determination of in situ hepatic malondialdehyde levels revealed a 2-fold increase in malondialdehyde content on day 30 following the Aroclor 1254 injection. Further, parallel increases in in situ malondialdehyde levels and ethane production rates were also found 30 days following a single IP injection of 3,3′,4,4′-tetrachlorobiphenyl, 2,3,4,4′,5-pentachlorobiphenyl and 2,2′,4,4′,5,5′-hexachlorobiphenyl (300 μmol/kg). These effects were not reflected in increased diene conjugation. Redox state of the liver was largely unaffected, as evidenced by the relative concentrations of reduced and oxidized NADPH. However, minor changes in reduced and oxidized glutathione were noted.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00293625
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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
    Pharmacokinetics of ethylene in man; body burden with ethylene oxide and hydroxyethylation of hemoglobin due to endogenous and environmental ethylene (1992)
    Springer
    Archives of toxicology 66 (1992), S. 157-163 
    Details
    ISSN: 1432-0738
    Keywords: Ethylene ; Ethylene oxide ; Pharmacokinetics ; Hemoglobin adduct ; Man
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The inhalation pharmacokinetics and the endogenous production of ethylene has been determined in healthy volunteers with respect to the formation of the carcinogen ethylene oxide. Ethylene showed a low degree of accumulation in the body determined in six subjects, the thermodynamic partition coefficient “body/air” being 0.53±0.23 (mean ± SD) and the accumulation factor “body/air” at steady-state being 0.33±0.13 (mean ± SD). The rate of metabolism was directly proportional to the exposure concentration. Only 2% of ethylene inhaled was metabolized to ethylene oxide, whereas 98% of ethylene was exhaled unchanged. The rate of the endogenous production of ethylene was 32±12 nmol/h (mean ± SD), as calculated from exhalation data from 14 subjects. The resulting body burden was 0.44±0.19 nmol/kg (mean ± SD). By analyzing published data on ethylene oxide in man its half-life was estimated to be 42 min. Using the pharmacokinetic parameters of ethylene and ethylene oxide, the body burden of ethylene oxide due to the sum of the exposure to environmental ethylene of about 15 ppb and to endogenous ethylene exposure of 0.44 nmol/kg was predicted to be 0.25 nmol/kg. In the blood of five nonsmokers and one smoker the hemoglobin adduct resulting from the reaction of ethylene oxide with the N-terminal valine, N-(2-hydroxyethyl)valine, was quantified by gas chromatography/mass spectrometry. The value of 20±5 pmol/g Hb (mean ± SD) found in the non-smokers corroborated the steady-state level of 18±3 pmol/g Hb (mean ± SD) calculated from the pharmacokinetic approach.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01974008
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  • 7
    Electronic Resource
    Electronic Resource
    Urinary excretion of acetylcyanamide in rat and human after oral and dermal application of hydrogen cyanamide (H2NCN) (1991)
    Springer
    Archives of toxicology 65 (1991), S. 268-272 
    Details
    ISSN: 1432-0738
    Keywords: Hydrogen cyanamide ; Rat ; Human ; Metabolism ; Urinary excretion ; Acetylcyanamide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The main urinary metabolite of hydrogen cyanamide (syn.: cyanamide) in rat and man is acetylcyanamide (syn.: N-acetylcyanamide). An analytical method was developed to determine acetylcyanamide in the urine with a limit of quantification of 〈10 μg/l (mean recovery 96.1 % using spikes of 20 μg/l; relative standard deviation 〈4%). This methodology is based upon ion chromatography using column-switch techniques and UV detection. It could be demonstrated that in rats an average of 45.6% of oral applied cyanamide (10 mg/kg) was excreted in the urine as acetylcyanamide. In male human volunteers a mean of 40% of oral administered cyanamide (mean dose 0.25 mg/kg body weight) was excreted via the urine as acetylcyanamide. The same group of volunteers participated in a skin absorption study with dermal application of the above cyanamide dose onto a skin surface area of 32 cm2. Within an application period of 6 h an average cyanamide quantity of 2.3 mg was available for skin absorption. A mean portion of 7.7% of this quantity was found as acetylcyanamide in the urine of the participants. Findings from literature state that cyanamide is metabolized in vitro to cyanide. According to examinations performed in vivo, however, such a metabolic pathway seems to be irrelevant for man. In comparison with the control values there was no significant increase of both the cyanide concentrations in the blood and the thiocyanate concentrations in the urine of the above volunteers after the described oral cyanamide administration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01968960
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  • 8
    Electronic Resource
    Electronic Resource
    Pharmacokinetics of ethylene in man; body burden with ethylene oxide and hydroxyethylation of hemoglobin due to endogenous and environmental ethylene (1993)
    Springer
    Archives of toxicology 67 (1993), S. 230-230 
    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/BF01973314
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  • 9
    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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  • 10
    Electronic Resource
    Electronic Resource
    Different pharmacokinetics of dichlorofluoromethane (CFC 21) and chlorodifluoromethane (CFC 22) (1986)
    Springer
    Archives of toxicology 58 (1986), S. 282-283 
    Details
    ISSN: 1432-0738
    Keywords: Pharmacokinetics ; Dichlorofluoromethane ; Chlorodifluoromethane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Inhalation pharmacokinetics of dichlorofluoromethane (CFC 21) and chlorodifluoromethane (CFC 22) were studied in male Wistar rats by use of a closed inhalation chamber system. CFC 21 was readily eliminated via metabolism. However, CFC 22 underwent no detectable metabolism; pretreatment of the rats with DDT or phenobarbital did not stimulate metabolic transformation of the compound. Hence, formation of biologically relevant amounts of reactive intermediates from CFC 22 as a mechanism of toxicity seems unlikely.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00297122
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