IMMOBILIZATION STRESS ENHANCES LIPID-PEROXIDATION IN THE RAT LUNGS

The present work was carried out to study the involvement of lipid per oxidation in immobilization-induced damage of the rat lung. Thirty-hou r 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 conjug ated dienes and fluorescent products of lipid peroxidation were measur ed in the lungs of rats immobilized over 12 h. Immobilization stress w as followed by significant changes in the fatty acid contents of lung phospholipids. The levels of polyunsaturated fatty acids C-18:2 (linol eic acid) and C-20:4 (arachidonic acid) were decreased even during the alarm phase. The contents of monounsaturated fatty acids did not chan ge, while those of saturated fatty acids slightly increased. The invol vement of lipid peroxidation in immobilization-induced damage of the r at lung was indirectly supported by the observation of decreased level s 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 pre ceded the immobilization stress-induced damage of the lung cell membra nes. Therefore, it seems likely that lipid peroxidation is the cause, rather than a consequence of the stress-altered lung structure.