The content of phospholipids and their fatty acid composition were followed in the hearts of two inbred strains of rats: IR, resistant against the development of isoprenaline-induced myocardial lesions and IS, sensitive to their development. In the hearts of rats of the resistant strain, a lower content of phosphatidylcholine and its plasmalogen fraction was found compared to IS rats. The total amount of phospholipids was only insignificantly lower in IR rats. Greater differences were found in individual fatty acids. The most important finding concerned lower arachidonic acid and higher linoleic acid content in heart phospholipids of IR rats. These differences were exactly opposite to changes reported in the literature in animals known to have a higher resistance against myocardial damage due to various interventions. Our results do not support the hypothesis claiming the importance of changes in phospholipids and their FA composition for the resistance of the heart against the development of necrotic lesions.
Sensitivity of various mitochondrial enzymes to oxidative damage was tested on isolated rat liver hepatocytes
permeabilized by digitonin. In permeabilized hepatocytes
normal respiratory control
values were obtained and
mitochondrial membranes remained intact. Respiratory rate
s of NADH-dependent (glutamate+malate, palmitylcarnitine
+ malate) and flavoprotein-dependent (succinate) substrates were determined in hepatocytes exposed for 5 min to
0.5-3 mM
tert
-butyl hydroperoxide before addition of digitonin.
Our data showed that oxidation of NADH-dependent
substrates is much more sensitive to oxidative stress than ox
idation of flavoprotein-dependent ones, evidently due to the
modification of iron-sulfur clusters or SH groups in the NADH dehydrogenase enzyme complex (Complex I).