Vitamin E, supplemented to semisynthetic or natural commercial diets in amounts of 60–180 mg/kg increased the humoral immune response of mice against sheep red blood cell or tetanus toxoid antigens by 30–40%, measured by the antibody plaque forming cell test, or by hemagglutination. Vitamin E affected particularly the IgG antibody production. The antioxidant NN-diphenyl-p-phenylene diamine was ineffective in restoring immune response in a vitamin E-deficient diet, and was only partially effective in replacing vitamin E in a normal diet.

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Immunoturbidimetric analysis of lipoprotein(a) in plasma or serum was developed for use on the Roche COBAS FARA II and COBAS MIRA clinical chemistry analyzers. The components of the assay are: (1) buffer consisting of 2.25% polyethylene glycol in phosphate-buffered saline, 0.2% gelatin, and a surfactant; (2) fractionated goat anti-human lipoprotein(a) IgG; (3) five standards with lipoprotein(a) concentrations ranging from 0.05 to 1.0 g/l; (4) two controls with concentrations of approximately 0.2 and 0.5 g/l. The analyzer delivers sample and buffer, incubates the reaction mixture at 37 degrees C for 5 min, delivers neat lipoprotein(a) antibody, and incubates for an additional 10 min. The lipoprotein(a) concentration of samples is calculated by the COBAS DENS (Data Evaluation for Non-linear Standard Curves) option by fitting the standard curve values to a four-parameter logit-log curve model. Total imprecision results (CV%) for the FARA II and MIRA were under 11% (NCCLS protocol EP5-T). The assay is linear beyond the highest calibrator to 2.6 g/l. No interference was observed for plasminogen up to 2.3 g/l, apolipoprotein B up to 4.36 g/l, hemoglobin up to 10 g/l, bilirubin up to 4.0 g/l, and triglycerides up to 4.36 g/l. Comparison with a double monoclonal ELISA used at the Northwest Lipid Research Laboratories yielded: R = 0.970, slope = 1.013, and y-intercept = 0.00009 (n = 37). Comparison with a commercially available ELISA kit for lipoprotein(a) yielded: r = 0.987, slope = 1.243, and y-intercept = 0.024 (n = 40). This assay provides rapid, accurate, and precise screening of lipoprotein(a) in serum or plasma.

Vitamin E protects nonimmunized and immunized mice against fatal Diplococcus pneumoniae type I (DpI) infection. A dietary supplementation of 180 mg of DL-a-tocopheryl acetate per kg of diet increased survival of nonimmunized mice from 20 to 80% when challenged with 20 organisms, and of mice immunized with 0.5 ng of DpI polysaccharide from 15 to 70% when challenged with 20,000 organisms. The phagocytic index of immunized mice was four times higher in the 180-mg vitamin E group than in the control group. Both the survival and phagocytic index revealed a biphasic dose response, indicating a cause-effect relationship between phagocytosis and survival. Vitamin E also significantly increased the rate of carbon clearance from blood, indicating a general increase in phagocytic activity. The data indicated that increased macrophage activity probably aided by increased antibody production was the principal reason for increased protection.

Chicks and hens raised on a diet enriched with 60 mg of vitamin E per lb. of feed had a significantly increased immune response as measured by the antibody plaque-forming cell test or by hemagglutination. Since the effect was much greater on hypoxic (simulated altitude exposed) chicks, a synergistic effect between hypoxia and vitamin E may be suggested.Vitamin E, which was first recognized as a fertility factor for rats (10) and is known as a powerful antioxidant (7), apparently has other important but less known functions. Among these functions may be the involvement in the cellular development of the hemopoietic-immunopoietic system, the cells of which most likely originate from a common pluripotential stem cell (12). The involvement of vitamin E in the development and population kinetics of erythroid cells has already been demonstrated (3,6,8 Fig. 1 that vitamin E significantly increased the number of AB PFC both at ground level (1,500 m) and at 4,800 m simulated altitude level. However, the great increase in PFC in the altitude group indicated that the effect of vitamin E and hypoxia was synergistic.The unusually high background counts in Fig. 1 as compared to those obtained by others (1) probably were due to the use of undiluted guinea pig complement and indicated a large percentage of nonspecifically reacting cells, which are most likely not precursors of PFC (5). Those cells which responded specifically to the SRBC immunogenic stimulus, however, gave significant differences within treatment groups and compared to the controls (P < 0.05). The background PFC counts among diet and altitude controls were not significantly different. The HA titers in these young chicks at this stage were too low to interpret correctly.The chicks were reimmunized at age 31 days, partly to see whether a residual effect of the hypoxic shock remained and partly to see the change in the secondary response. Figure 2 shows the result of an indirect PFC test, showing that (i) the previous hypoxic shock had no