The Association of Halothane-Induced Lipid Peroxidation with the Anaerobic Metabolism of Halothane : An In Vitro Study in Guinea Pig Liver Microsomes

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Title ( eng )
The Association of Halothane-Induced Lipid Peroxidation with the Anaerobic Metabolism of Halothane : An In Vitro Study in Guinea Pig Liver Microsomes
Creator
Sato Nobuyoshi
Fujii Kohyu
Yuge Osafumi
Morio Michio
Source Title
Hiroshima Journal of Medical Sciences
Volume 39
Issue 1
Start Page 1
End Page 6
Journal Identifire
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
Abstract
The formation of pentane and anaerobic metabolites of halothane (2-chloro-1,1,1-trifluoroethane and 2-chloro-1,1-difluoroethylene) in a mixture of guinea pig liver microsomes and halothane (2-bromo-2-chloro-1,1,1-trifluoroethane) in the presence of NADPH was studied by gas chromatography. Under anaerobic conditions, pentane was formed without halothane and was inhibited by oxygen tension. This anaerobic pentane formation was potentiated 2.5 times by addition of halothane. Halothane-induced pentane formation increased dose-dependently with a halothane concentration of up to 2.1 mmol/liter and then decreased in the presence of increasing concentrations of halothane. Inhibition by a higher substrate was also observed in the formation of anaerobic metabolites of halothane. Antioxidant agents, vitamin E and glutathione, reduced the pentane formation, but did not reduce the anaerobic metabolites of halothane. Metyrapone, an inhibitor of cytochrome P-450, reduced both the pentane and anaerobic metabolites of halothane. These results show holothane-induced lipid peroxidation in association with the anaerobic metabolism of halothane in guinea pig liver microsomes.
Keywords
Halothane
Microsome
Liver
Lipid peroxides
Pentane
Descriptions
This study was supported in part by a Grant-in-aid for Science Research from the Ministry of Education, Science and Culture of Japan.
NDC
Medical sciences [ 490 ]
Language
eng
Resource Type departmental bulletin paper
Publisher
Hiroshima University Medical Press
Date of Issued 1990-03
Publish Type Version of Record
Access Rights open access
Source Identifier
[ISSN] 0018-2052
[NCID] AA00664312
[PMID] 2373636