Vitamin E deficiency and erythrocyte deformability in the rat

Abstract

It has been suggested that erythrocyte deformability is decreased in vitamin E deficiency due to oxidative damage to the cell membrane. Male Wistar rats (66 to 88 g) were fed ad libitum an AIN76-based diet containing tocopherol-stripped corn oil without added vitamin E for 8 weeks (−E; n = 8). Control animals were fed ad libitum the same diet containing 50 IU/kg dl-α-tocopheryl acetate (+E; n = 7). Vitamin E deficiency was confirmed by depressed mean (±SEM) plasma α-tocopherol levels (μmol/L), as measured by high performance liquid chromatography [−E: 0.5 ± 0.1; +E: 20.3 ± 1.8] and elevated hydrogen peroxide-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 count was a depression in reticulocyte number (× 10 12/L) [−E: 0.19 ± 0.02; +E: 0.46 ± 0.03; P < 0.05]. Erythrocyte deformability was measured at standard shear stress under conditions of increasing osmolality in the ektacytometer. Elongation index (the ratio of length to width of the diffraction pattern of the deformed cells) was plotted against osmolality to generate an osmotic deformability profile. EI max (the maximum elongation index) and O hyper (the osmolality at which the elongation index is half of EI max on the hypertonic arm of the 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 vitamin E deficiency in the rat. In fact, a small but significant increase in maximum deformability was observed in erythrocytes from vitamin E-deficient rats.