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The effects of beta-carotene, retinol, and retinoic acid on function of mononuclear cells during the peripartum period was assessed in vitro. Blood was collected from 14 Holstein cows on wk -4, -1, 0, 1, and 4 postpartum, and mononuclear cells were obtained by gradient centrifugation. Mononuclear cell proliferation induced by concanavalin A was measured in the presence of beta-carotene, retinol (1 x 10(-9) and 1 x 10(-8) M), and retinoic acid (1 x 10(-10) and 1 x 10(-9) M). Retinol and beta-carotene had no effect on spontaneous cell proliferation, whereas retinoic acid was suppressive. However, 1 x 10(-9) M beta-carotene enhanced concanavalin A-induced proliferation at wk -1, whereas 1 x 10(-8) M beta-carotene was suppressive at wk -4. Retinoic acid suppressed concanavalin A-induced proliferation at wk 0, but retinol had no effect. These results suggest a mechanism by which beta-carotene affords the mammary gland protection against infection immediately prepartum.

The effects of in vitro supplementation of beta-carotene, retinol, and retinoic acid on phagocyte function during the peripartum period were assessed. Blood was collected at wk -4, -1, 0 (calving), 1, and 4; mammary secretions were collected at wk -1, 0, 1, and 4 from 14 Holstein cows for the isolation of phagocytic cells. Blood polymorphonuclear leukocytes and mammary macrophages and polymorphonuclear leukocytes (phagocytic cells) were assayed for phagocytic and intracellular kill abilities of Staphylococcus aureus in the presence of beta-carotene and retinol at 10(-8) and 10(-7) M and retinoic acid at 10(-9) and 10(-8) M. Phagocytosis by blood or milk phagocytic cells was not influenced by beta-carotene. However, beta-carotene enhanced kill by blood and milk phagocytic cells during certain prepartum and post-partum periods. In contrast to beta-carotene, retinol and retinoic acid either had no effect or suppressed phagocytosis and kill. These results are interpreted to suggest a mechanism by which beta-carotene affords the mammary gland protection against infection, i.e., through enhanced intracellular kill by phagocytes.

Vitamin A and beta-carotene improved mammary health in dairy cows around dry off. To define possible mechanisms, cows were fed 1) 53,000 IU vitamin A, 2) 213,000 IU vitamin A, or 3) 53,000 IU vitamin A plus 400 mg beta-carotene/cow per d (n = 10/treatment) from 6 wk before to 2 wk after dry off. Blood polymorphonuclear neutrophil function (phagocytosis, kill, and chemotaxis) and lymphocyte proliferation were measured at wk -6, 0 (dry off), and 2. Concentrations of vitamin A in serum did not differ across vitamin treatments. beta-Carotene in serum was elevated in cows fed beta-carotene. Treatment did not influence phagocytosis or kill. Kill ability increased after dry off in all treatment groups, but phagocytosis tended to decrease after dry off in cows fed vitamin A only. Lymphocyte blastogenesis stimulated by concanavalin A on wk 2 for cows fed 53,000 IU vitamin A but did not vary in the other two groups. Lipopolysaccharide-stimulated blastogenesis peaked at wk 0 and then decreased to pretreatment values by wk 2 in cows fed 213,000 IU vitamin A. These data indicate lymphocyte function is influenced by vitamin A supplementation and that beta-carotene supplementation seems to exert a stabilizing effect on neutrophil and lymphocyte function during the period around dry off.

The interaction of dietary vitamin A and beta-carotene with lactational status on the in vitro proliferation of mitogen-induced peripheral blood lymphocytes was studied. Cows were fed (IU/cow per d) 1) 53,000 IU vitamin A, 2) 213,000 IU vitamin A, or 3) 53,000 IU vitamin A plus 400 mg beta-carotene from 6 wk before to 2 wk after dry off. Lymphocytes were incubated with retinol, retinoic acid, or beta-carotene. Concanavalin A-induced blastogenesis was inhibited by 10(-6) M retinol and 10(-8) M retinoic acid in cows fed 53,000 IU vitamin A before dry off. In contrast, 10(-7) M retinol and 10(-7) M retinoic acid stimulated Concanavalin A-induced blastogenesis for cows fed vitamin A plus beta-carotene before dry off. After dry off, retinol and retinoic acid did not affect Concanavalin A-induced blastogenesis in all treatment groups. In vitro, 10(-5) M beta-carotene inhibited Concanavalin A-induced blastogenesis before and after dry off in all treatment groups. Blastogenesis in the absence of mitogen stimulation or induced by lipopolysaccharide was inhibited by all vitamins before and after dry off in all treatment groups. These data indicate that vitamin A and beta-carotene supplementation interact with lactational status to influence the responsiveness of bovine blood lymphocytes to vitamin challenge in vitro.

L-Arginine or saline was administered intravenously by rapid infusion into 16 late-pregnant Holstein cows to study changes of prolactin, growth hormone, insulin, total protein, urea nitrogen, and subsequent lactation. Arginine was infused daily at .1 g/kg body weight starting about 7 days prior to predicted calving until calving. Blood was sampled via a jugular cannula at 0700, 0715, 0730 (infusion immediately followed 0730 h sample), 0745, 0815, 0845, 1100, 1300, 1500, 1700, and 1900 h. Arginine infusion evoked dramatic but transient increase of concentrations of blood serum prolactin, growth hormone, and insulin. Urea nitrogen also was elevated in blood serum but not total protein. The secretory response of prolactin, growth hormone, and insulin to daily arginine infusion during the entire prepartum period was not diminished. Milk production for the first 22 wk of lactation tended to be higher (by about 10%) for cows infused with arginine as compared to cows infused with saline. Therefore, repeated arginine infusion in late-pregnant cows dramatically increased prolactin, growth hormone, and insulin and tended to increase subsequent milk yield.

Antimicrobial activities of three phenolic compounds and four metal chelators were tested at 0, 250, 500, and 1000 ppm in vitro against four major mastitis-causing bacteria, Streptococcus agalactiae, Staphylococcus aureus, Klebsiella pneumoniae, and Escherichia coli. Overall, butylated hydroxyanisole and tert-butylhydroquinone showed the greatest antimicrobial activity. These phenolics were bactericidal at 250 to 500 ppm against all four bacteria tested. The butylated hydroxytoluene was bactericidal against the gram-positive bacteria but was ineffective against the coliforms. At 250 ppm, disodium ethylenediaminetetraacetic acid was bactericidal against the gram-positive bacteria but much less effective against the gram-negatives. However, diethylenetriaminepentaacetic acid was more growth inhibitory than ethylenediaminetetraacetic acid against the gram-negative bacteria and especially against Escherichia coli. All other compounds were generally much less effective or ineffective against all four microorganisms. Therefore, butylated hydroxyanisole, butylated hydroxytoluene, tert-butylhydroquinone, ethylenediaminetetraacetic acid, and diethylenetriaminepentaacetic acid may have practical implications in the prevention or treatment of bovine mastitis.

Dietary vitamin A and beta-carotene were assessed on their interaction with lactational status to influence neutrophil function in vitro. Cows were fed 1) 53,000 IU or 2) 213,000 IU vitamin A, or 3) 53,000 IU vitamin A plus 400 mg beta-carotene/cow per d from 6 wk before to 2 wk after dry off. Blood neutrophils were isolated the day of dry off and 2 wk after dry off and incubated with retinol, retinoic acid, or beta-carotene. Phagocytosis and kill of Staphylococcus aureus were measured. Across all treatments, kill was higher after dry off than before dry off. Phagocytosis tended to be lower after dry off than before in cows fed vitamin A only. In vitro, 10(-6) M beta-carotene stimulated phagocytosis after dry off and kill before dry off in cows fed vitamin A only. In general, retinol and retinoic acid suppressed phagocytosis but did not affect kill. Neutrophils from cows fed high amounts of vitamin A were more susceptible to in vitro suppression than those from cows fed adequate amounts of vitamin A. Therefore, vitamin A and beta-carotene supplementation interacts with lactational status to influence the responsiveness of bovine neutrophils to vitamin challenge in vitro.