Metabolism of 4-Hydroxynonenal, a Cytotoxic Lipid Peroxidation Product, in Thymocytes as an Effective Secondary Antioxidative Defense Mechanism

The metabolism of the aldehydic lipid peroxidation product, 4-hydroxynonenal (HNE), was studied in suspensions of mouse thymocytes. Thymocytes are characterized by low lipid peroxidation in comparison with other cell types notwithstanding their high content of arachidonic acid. In our study a very h...

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Published in:Journal of biochemistry (Tokyo) Vol. 123; no. 3; pp. 534 - 539
Main Authors: Siems, Werner G., Pimenov, Alexej M., Esterbauer, Hermann, Grune, Tilman
Format: Journal Article
Language:English
Published: England Oxford University Press 01-03-1998
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Summary:The metabolism of the aldehydic lipid peroxidation product, 4-hydroxynonenal (HNE), was studied in suspensions of mouse thymocytes. Thymocytes are characterized by low lipid peroxidation in comparison with other cell types notwithstanding their high content of arachidonic acid. In our study a very high capacity of HNE metabolism in thymocytes was observed: 27.7 nmol/mg w.w./min. That is about the same HNE degradation rate as determined in liver cells or small intestinal enterocytes, which are the cells with the by far highest capacity for the degradation of HNE and other aldehydic lipid peroxidation products in comparison with other cell types. The primary and secondary HNE metabolites in thymocytes were identified and quantified after the addition of 100 μM HNE to thymocyte suspensions: the glutathione-HNE conjugate, the hydroxynonenoic acid, the 1,4-dihydroxynonene, water, and the glutathione-dihydroxynonene conjugate. Furthermore, the HNE binding to proteins was measured. The very rapid HNE degradation in thymocytes besides the high amounts of lipophilic chain-breaking antioxidants is postulated to be an important secondary antioxidative mechanism and the main factor for the low accumulation of lipid peroxidation products in these cells.
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ArticleID:123.3.534
1 These investigations were supported by grants from the Deutsche Forschungsgemeinschaft, Grants Gr 1240/3–1 (T.G.) and Si 619/1–1 (W.G.S.). The paper is dedicated to our coauthor and friend, the former head of the Institute of Biochemistry at the University of Graz, Austria, Prof. Hermann Esterbauer (1936–1997). The authors are greatly indebted to this leading scientist in the field of free radical research, especially in the fields of lipid peroxidation, its clinical importance, and cytotoxic lipid peroxidation products.
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ISSN:0021-924X
DOI:10.1093/oxfordjournals.jbchem.a021969