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Beginning 4 wk prior to predicted calving, 14 Holstein cows per treatment were fed diets 1) unsupplemented (control) or supplemented daily with 2) 300 mg of beta-carotene, 3) 600 mg of beta-carotene, or 4) 120,000 IU of vitamin A. Blood was collected around calving on wk -4, -2, -1, 0 (within 24 h postcalving), 1, 2, and 4 for isolation of lymphocytes and neutrophils and for the analysis of plasma vitamins. Lacteal secretions were collected on wk 0, 1, 2, and 4 for the isolation of phagocytes. Cows supplemented with 600 mg of beta-carotene had higher concentrations of plasma beta-carotene and retinol than did unsupplemented cows. Supplemental vitamin A increased plasma retinol on wk 4 and decreased plasma beta-carotene on wk -1 and 0. Treatment did not affect concentrations of plasma alpha-tocopherol. Blood lymphocyte proliferation in response to concanavalin A, phytohemagglutinin, and pokeweed mitogen during the peripartum period was higher in cows supplemented with beta-carotene than in unsupplemented controls. Phagocytic activity of blood neutrophils was enhanced on wk 1 in cows fed 300 mg of beta-carotene. Intracellular killing by blood neutrophils was enhanced in cows supplemented with beta-carotene (wk 0) and vitamin A (wk 0 and 1). Iodine uptake and nitroblue tetrazolium reduction by blood neutrophils was stimulated in cows supplemented with beta-carotene. Phagocytic activity, iodine uptake, and nitroblue tetrazolium reduction by mammary phagocytes from all cows generally were lower postpartum than on the day of calving. The incidence of retained placenta and metritis was higher for unsupplemented cows than for cows supplemented with beta-carotene. Therefore, dietary beta-carotene can elevate peripartum concentrations of blood beta-carotene, enhance host defense mechanisms by potentiating lymphocyte and phagocyte function, and decrease the incidence of certain reproductive disorders.

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High levels of dietary lutein can inhibit mammary tumor growth in mice. However, the antitumor effect of low levels of dietary lutein on mammary tumors is unavailable. Female BALB/c mice and the WAZ-2T (-SA) mammary tumor cell line were used in two experiments. A preliminary tumor cell dose titration study (Experiment 1) was designed to determine the inoculation dose to produce approximately 65% tumor incidence. Mice (n = 10/dose) were inoculated with 0 to 1 x 10(6) tumor cells in the right inguinal mammary fat pad. A tumor cell load of 2.5 x 10(3) cells/inoculation produced approximately 65% tumor incidence. This dose was used in a subsequent study (Experiment 2) of the efficacy of dietary lutein against mammary tumor development. Mice (n = 20/treatment) were fed a semisynthetic diet containing 0, 0.002, 0.02, 0.2 or 0.4% lutein from marigold extract. After 14 d, all mice were inoculated with 2.5 x 10(3) tumor cells, and tumor growth was measured daily for 70 d at which time blood, liver, spleen and tumors were obtained. Lutein + zeaxanthin uptake increased dose-dependently (P < 0.05) with dietary lutein levels from 0 to 0.02% (spleen) or 0.2% (plasma, liver and tumor). Low levels (0.002 and 0.02%) of dietary lutein lowered (P < 0.05) mammary tumor incidence, tumor growth and lipid peroxidation, and increased tumor latency, whereas higher dietary levels (0.2 or 0.4%) were less effective. Therefore, very low amounts of dietary lutein (0.002%) can efficiently decrease mammary tumor development and growth in mice.

The uptake of beta-carotene by blood cells, plasma, and lipoproteins was studied in bull calves that were orally administered a single (Exp. 1; n = 18 Angus calves) or multiple (Exp. 2; n = 16 Holstein calves) doses of beta-carotene. Administration of beta-carotene increased plasma beta-carotene and the amount of beta-carotene associated with each lipoprotein fraction. Before beta-carotene treatment, the total amount of beta-carotene associated with the high-density lipoprotein (HDL) was three- to fourfold higher than the amount associated with low-density lipoprotein (LDL) and fivefold higher than the amount associated with very-low-density lipoprotein (VLDL). The relative increase in total beta-carotene associated with the lipoproteins was greater for LDL than for HDL or VLDL. Orally administered beta-carotene increased the uptake of beta-carotene by lymphocytes. Subcellular fractions of blood lymphocytes isolated from animals fed beta-carotene revealed that beta-carotene was taken up in significant amounts by the mitochondrial, nuclear, and microsomal fractions. The profile of beta-carotene uptake by these subcellular fractions did not mirror that observed in plasma. In contrast, beta-carotene was not detectable in blood neutrophils and erythrocytes in either beta-carotene-supplemented or unsupplemented calves. Treatment did not influence the concentrations of retinol or alpha-tocopherol in plasma, lipoproteins, lymphocytes, neutrophils, or erythrocytes. These data revealed the presence of beta-carotene in bovine lymphocyte subcellular fractions and suggest a possible physiological role of beta-carotene in these cells.