INFLUENCE OF VITAMIN-E SUCCINATE ON RETINAL CELL-SURVIVAL

In this study, we analyzed the influence of vitamin E succinate (5-80 mu M), supplemented in the culture medium, on the survival of cultured retinal cells. The release of lactate dehydrogenase (LDH) was decreas ed in the presence of low concentrations (10-20 mu M) of vitamin E suc cinate, whereas high concentrations (80 mu M) induced a significant in crease (about 2-fold) in the release of LDH, indicating a reduction of plasma membrane integrity. Supplementing with vitamin E succinate (80 mu M) greatly enhanced its cellular content, as compared to vitamin E acetate (80 mu M), and the membrane order of the retinal cells, as ev aluated by the fluorescence anisotropy (r) of TMA-DPH ethylammonium)-p henyl)-6-phenylhexa-1,3,5-triene), was not altered. Furthermore, vitam in E succinate was more potent than vitamin E acetate in reducing thio barbituric acid reactive substances (TBARS) formation upon ascorbate-F e2+-induced oxidative stress (TBARS formation after cell oxidation dec reased by about 15-fold or 1.6 fold, respectively, in the presence of 20 mu M vitamin E succinate or 20 mu M vitamin E acetate). A decrease in MTT (4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) red uction induced by supplementing with vitamin E succinate (80 mu M), to 35.99 +/- 1.96% as compared to the control, but not by vitamin E acet ate (80 mu M), suggests that vitamin E succinate may affect the mitoch ondrial activity. Vitamin E succinate also reduced significantly the A TP:ADP ratio in a dose-dependent manner, indicating that vitamin E suc cinate-mediated cytotoxic effects involve a decrement of mitochondrial function. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.