ALPHA-TOCOPHEROL UPTAKE AND ITS INFLUENCE ON CELL-PROLIFERATION AND LIPID-PEROXIDATION IN TRANSFORMED AND NONTRANSFORMED BABY HAMSTER-KIDNEY CELLS

α-Tocopherol (α-T) uptake and its relationship to cell proliferation and lipid peroxidation was studied in a baby hamster kidney cell line (BHK-21/C13) and its polyoma virus-transformed malignant counterpart (BHK-2 1/PyY cells). The principal findings were as follows. (i) The level of lipid peroxidation, judged by malondialdehyde (MDA) measurement by HPLC, was higher in the transformed cells than in the nontransformed cells. Oxidative stress by 374 μM Fe3+/10 mM ADP caused a significant increase in the level of MDA of a similar magnitude in both cell types. Addition of 7, 14, and 21 μM α-T caused no diminution of the MDA level in the unstressed cells and abolished the rise in MDA seen in the stressed cells. (ii) The endogenous level of α-T in the transformed cells was lower than in the nontransformed cells and all the measurable α-T in these cells was destroyed by the oxidative stress. Supplementation of the cells with α-T caused a rise in the level of α-T proportional to the level of inclusion of α-T in the medium. (iii) α-Tocopheryl quinone in the transformed cells was unaffected by oxidative stress and in the nontransformed cells stress caused a large increase in this metabolite when α-T was included at the 21 μM level. (iv) Growth was stimulated by 7 and 14 μM α-T but not by the higher level of inclusion in the medium. The growth stimulation was much larger in the transformed cells (163% of growth in the unsupplemented medium) than in the nontransformed cells (120%). (v) These results demonstrate that, in this cell system, the growth-stimulating ability of α-T is unrelated to the ability of α-T to control lipid peroxidation and that the level of peroxidation is increased in the malignant state. © 1993 Academic Press, Inc.