VITAMIN-E-DEFICIENCY AND ERYTHROCYTE DEFORMABILITY IN THE RAT

It has been surrogated that erythrocyte deformability is decreased in vitamin E deficiency due to oxidative damage to the cell membrane. Mal e Wistar rats (66 to 88 g) were fed ad libitum an AlN76-based diet con taining tocopherol-stripped corn oil without added vitamin E for 8 wee ks (- E; n = 8). Control animals were fed ad libitum the same diet con taining 50 IU/kg dl-alpha-tocopheryl acetate (+ E; n = 7). Vitamin E d eficiency was confirmed by depressed mean (+/- SEM) plasma alpha-tocop herol levels (mu mol/L), as measured by high performance liquid chroma tography [- E: 0.5 +/- 0.1; + E: 20.3 +/- 1.8] and elevated hydrogen p eroxide-induced hemolysis (%) [- E: 92.6 +/- 2.4; + E: 4.2 +/- 1.6; P < 0.05 by Student's t test]. The only alteration in a complete blood c ount was a depression in reticulocyte number (X 10(12)/L) [- E: 0.19 /- 0.02; +/- E: 0.46 +/- 0.03; P < 0.05]. Erythrocyte deformability M as measured at standard shear stress wirier conditions of increasing o smolality in the ektacytometer. Elongation inde?e (the ratio of length to width of the diffraction pattern of the deformed cells) was plotte d against osmolality to generate an osmotic deformability profile. EI( max) (the maximum elongation index) and O-hyper (the osmolality at whi ch the elongation index is half of EI(max) on the hypertonic arm of th e curve) were significantly increased in samples from the - E group (P < 0.05 by Student's t test). In summary, erythrocyte deformability as measured by the ektacytometer was not decreased by a subclinical vita min E deficiency in the rat. In fact, a small but significant increase in maximum deformability was observed in erythrocytes from vitamin E- deficient rats.