Lipid binding in mitochondria from testes of normal and essential fatty acid deficient rats.

Abstract

AbstractEssential fatty acid (EFA) deficiency in rat causes severe degeneration of spermatogenic tissue. Previously it was shown that the distribution of lipid classes changes very little during tissue degeneration. However it is well known that the fatty acid spectrum in lipids from testicular tissue is altered drastically during EFA deficiency. The molecular binding of lipids in membrane structures might be altered when a larger amount of ω9‐acids is present in the various lipid classes in testes of EFA‐deficient rats. In the present studies comparison was made of the binding of lipids in testicular mitochondrial membranes from rats fed a fat‐free diet or a diet containing 6% peanut oil for 26 weeks. Isolated mitochondria were coated on glass beads, then dried and packed into a column, whereafter the membrane lipids were eluted with solvents with increasing dielectric constants. The differences between the binding of lipid classes in supplemented and EFA‐deficient rats were not pronounced, but a tendency to a weaker binding in the EFA‐deficient rats was observed. However for both groups the various extracts showed marked differences in the distribution of lipid classes concurrent with the change of the eluent. This indicates a different kind of binding in the membrane, not only for different lipid classes, but also within a special lipid class. Thus both phosphatidylcholines (PC) and phosphatidylethanolamines (PE) were found in extracts with quite different dielectric constants. The fatty acid composition of PC and PE in the major fractions eluted with chloroform and ethanol, respectively, was essentially the same. This indicates that the successive release of phospholipids (PL) in these two fractions was not based on fatty acid solubility properties but on variable binding in the membrane structure. The introduction of ω9‐polyenoic fatty acids instead of ω6‐polyenoic fatty acids in the PL of mitochondria membranes from EFA‐deficient rats seems to be the only deviation in the lipid pattern of EFA‐supplemented and EFA‐deficient animals, and might therefore be responsible for the symptons of EFA deficiency.