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Gen Physiol Biophys. 1994 Dec;13(6):469-82.

Immobilization stress enhances lipid peroxidation in the rat lungs. Materials and methods.

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Sofia University School of Medicine, Department of Biophysics, Bulgaria.


The present work was carried out to study the involvement of lipid peroxidation in immobilization-induced damage of the rat lung. Thirty-hour immobilization stress was found to result in a marked morphological alteration of the lung ultrastructure and in significant increases of both acid and alkaline phosphatase for immobilization times exceeding 12 and 24 hours respectively. Also, increased concentrations of conjugated dienes and fluorescent products of lipid peroxidation were measured in the lungs of rats immobilized over 12 h. Immobilization stress was followed by significant changes in the fatty acid contents of lung phospholipids. The levels of polyunsaturated fatty acids C-18:2 (linoleic acid) and C-20:4 (arachidonic acid) were decreased even during the alarm phase. The contents of monounsaturated fatty acids did not change, while those of saturated fatty acids slightly increased. The involvement of lipid peroxidation in immobilization-induced damage of the rat lung was indirectly supported by the observation of decreased levels of vitamin E at 12 h immobilization. All the above data suggest that lipid peroxidation is somehow involved in the immobilization-induced damage of the rat lung. The observed changes in lipid peroxidation preceded the immobilization stress-induced damage of the lung cell membranes. Therefore, it seems likely that lipid peroxidation is the cause, rather than a consequence of the stress-altered lung structure.

[Indexed for MEDLINE]

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