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  • 1
    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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  • 2
    Electronic Resource
    Electronic Resource
    Cis- and trans-1,2-diphenylaziridines: induction of xenobiotic-metabolizing enzymes in rat liver and mutagenicity in Salmonella typhimurium (1986)
    Springer
    Archives of toxicology 59 (1986), S. 242-248 
    Details
    ISSN: 1432-0738
    Keywords: cis- and trans-stilbene imine ; cis- and trans-stilbene oxide ; Acenaphthene 1,2-imine ; Drug-metabolizing enzymes ; Mutagenicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract trans-Stilbene imine (trans-1,2-diphenylaziridine) is the nitrogen analog of trans-stilbene oxide, a potent inducer of several microsomal and cytosolic xenobiotic-metabolizing enzymes. Although the acute toxicity of cis- and trans-stilbene imines prevents their application at the usual dose for trans-stilbene oxide (400 mg/kg/day), it is apparent that the imines nevertheless potently induce several xenobiotic-metabolizing enzymes in rat liver. The IP administration of trans-stilbene imine resulted in statistically significant increases in the activities of aminopyrine N-demethylase, microsomal epoxide hydrolase, glutathione transferase (toward 1-chloro-2,4-dinitrobenzene, 1,2-dichloro-4-nitrobenzene and Δ5-androstene-3,17-dione) and UDP-glucuronosyltransferase (toward testoster-one). cis-Stilbene imine was less potent in inducing these activities. Although trans-stilbene imine (total dose = 400 mg/kg) was more potent than trans-stilbene oxide (total dose = 1200 mg/kg) in inducing the activities of glutathione transferase (toward 1-chloro-2,4-dinitrobenzene) and UDP-glucuronosyltransferase (toward testosterone), both compounds belong to the class of substances which are more potent inducers of conjugating (phase II) enzymes. Because of their structural similarity with K-region arene imines which are potent mutagens, cis-stilbene imine and trans-stilbene imine were investigated for mutagenicity (reversion of his − strains of Salmonella typhimurium). cis-Stilbene imine and trans-stilbene imine were direct mutagens in the strain TA100. This result, and the finding that acenaphthene 1,2-imine efficiently reverts various strains of Salmonella typhimurium, demonstrates that not only K-region arene imines, but also other aziridines substituted at the two carbons with aromatic moieties, are mutagenic.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00290545
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  • 3
    Electronic Resource
    Electronic Resource
    Absence of lipid peroxidation as determined by ethane exhalation in rats treated with 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) (1985)
    Springer
    Archives of toxicology 57 (1985), S. 13-16 
    Details
    ISSN: 1432-0738
    Keywords: Ethane exhalation ; TCDD-Rats ; Lipid peroxidation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The exhalation of ethane is widely used as an indicator of in vivo lipid peroxidation. To test the hypothesis that lipid peroxidative events are involved in the toxicity of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD), we administered a lethal dose of TCDD (60 μg/kg), IP to male Sprague Dawley rats (160–180 g) and measured by gas chromatography the exhalation of ethane into the atmosphere of a closed all-glass exposure chamber. TCDD-treated rats exhaled only slightly more ethane than control rats at a single time point 7 days following TCDD administration. Since the exhalation of ethane is the net result of the endogenous production of the gas and its metabolic degradation, the latter was quantified by measuring the clearance of exogenous ethane (initial concentration = 100 ppm) introduced to the atmosphere of the exposure chamber. The clearance of ethane in TCDD-treated rats was markedly decreased, reaching a minimum 7 days following TCDD treatment. Apparently, the slight increase in exhaled ethane was due to an inhibition of ethane metabolism caused by TCDD. However, rats obviously intoxicated and having lost considerable body weight might be impaired in their ability to transport ethane. To bypass this problem we injected ethane (0.2 ml) directly into the rats IP. Here also the metabolic clearance in TCDD-treated rats was diminished. In a further experiment, rats treated with dithiocarb at a dose where ethane metabolism was totally inhibited exhaled more ethane than did TCDD-treated rats. It is therefore concluded that the slight increase in ethane exhalation following a lethal dose of TCDD is due to a partial inhibition of ethane metabolism and that there is no net increase in ethane production due to lipid peroxidation. Indeed when TCDD-treated rats were administered Fe++, a well-known initiator of lipid peroxidation, they were less competent to carry out lipid peroxidation than rats treated with Fe++ alone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00286568
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  • 4
    Electronic Resource
    Electronic Resource
    Microbiological oxidation of the pentyl side chain of cannabinoids (1978)
    Springer
    Cellular and molecular life sciences 34 (1978), S. 1020-1022 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Syncephalastrum racemosum ATCC 18192 andMycobacterium rhodochrous ATCC 19067 partially degrade the n-pentyl side chain of cannabidiol, cannabinol, Δ8-tetrahydrocannabinol and Δ9-tetrahydrocannabinol. Carboxylic acid and alcohol side chain derivatives are major metabolites.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01915321
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