Accumulation of (E)-4-Hydroxy-2-nonenal and n-Hexanal, Degradation Products of Lipid Peroxides, in Mouse Lung and Liver
Effects of lipid peroxide breakdown products, (E)-4-hydroxy-2-nonenal (4-HN) and n-hexanal, on mouse lung lesion were examined. When 4-HN was injected i.v., the plasuma level of 4-HN increased just after the injection and then decreased immediately. The amounts of 4-HN increased in the liver and lun...
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Published in | Biological & pharmaceutical bulletin Vol. 16; no. 1; pp. 84 - 86 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Tokyo
The Pharmaceutical Society of Japan
01.01.1993
Maruzen Japan Science and Technology Agency |
Subjects | |
Online Access | Get full text |
ISSN | 0918-6158 1347-5215 |
DOI | 10.1248/bpb.16.84 |
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Summary: | Effects of lipid peroxide breakdown products, (E)-4-hydroxy-2-nonenal (4-HN) and n-hexanal, on mouse lung lesion were examined. When 4-HN was injected i.v., the plasuma level of 4-HN increased just after the injection and then decreased immediately. The amounts of 4-HN increased in the liver and lung were ca. 0.085 and 0.43% to the dose administered, respectively, 5min after the injection. Reduced glutathione (GSH) content and both GSH peroxidase (GSH-Px) and GSH reductase (GSSGR) activities in the lung were decreased significantly by 4-HN treatment. On the other hand, in the case of i.v. injection of n-hexanal into mice, the amount of n-hexanal detected in the lung was 5.0% to that of 4-HN, and no effect on the activities of GSH-Px and GSSGR and the content of GSH was observed.These results suggest that 4-HN generated from lipid peroxides would be transferred into the lung and cause the lung lesion through the inhibition of GSH-dependent antioxidative defense systems. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 0918-6158 1347-5215 |
DOI: | 10.1248/bpb.16.84 |