ABSTRACT
Table 1 ACCUMULATION OF PRODUCTS OF THE ENDOGENOUS LPO, CHANGES IN
THE PHOSPHOLIPID COMPOSITION, AND FUNCTIONAL DISTURBANCES IN THE SARCOPLASMIC RETICULUM MEMBRANES FROM SKELETAL
MUSCLES OF RATS IN THE COURSE OF THE DEVELOPMENT OF VITAMIN E DEFICIENCY"
in the cell, its role as antioxidant is considered to be the most probable."-M Repeated attempts have been made to detect experimentally the accumulation of lipid peroxides in the tissues of animals subjected to vitamin E-deficient diet. Although the earlier publications reported L P 0 activation in the course of E avitamin~sis,~ ' these results were not verified, which gave grounds for doubts about the real antioxidant action of vitamin E in the tissue^.^^.^^ Such controversy in the results of the analysis of L P 0 products in cases of vitamin E deficiency is caused by the inadequate methods applied for quantitative determination of lipid peroxides in the tissues and in their membrane structures in v i v ~ . ~ ~
The results of the determination of L P 0 products in sarcoplasmic reticulum membranes, isolated from the skeletal muscles of rats kept on vitamin E-deficient diet (Table l ) , show the in vivo accumulation of polarographically identified hydroperoxides, as well as of fluorescent Schiff bases (which are the end products of LPO), in the phospholipids of the sarcoplasmic reticulum, depending on the development of alimentary E avitaminosis. Induction of vitamin E deficiency for 60 days leads to reduction of the quantity of phosphatidylethanolamine, which is the main L P 0 substrate in biomembranes. Moreover, no regular changes in the endogenous level of MDA (TBA-reactive substances) are manifested. It may be concluded that the method with TBA is not suitable for assessing the content of L P 0 products in vivo, which probably gave rise to the contradictory results of the determination of the L P 0 products in the case of vitamin E d e f i ~ i e n c y . ~ ~ . ~ ~ The accumulation of lipid peroxides in various tissues during E avitaminosis has been verified repeatedly recently by means of adequate methods of determination of L P 0
Ca2 + transport is inhibited (the Ca2 'IATP ratio decreases) in the course of E avitaminosis. The Ca2+/ATP ratio decreases to zero after subjecting the animals to vitamin E-deficient diet, which is evidence of complete inhibition of the Ca2+ transport. The Ca2+-ATPase activity changes insignificantly within this period (Table 1).
