The effect of vitamin E derivatives on the urokinase-plasminogen activator (u-PA) system of resting and phorbol myristate acetate (PMA)-activated ovine macrophages and neutrophils were investigated. Blood monocyte -macrophages and neutrophils were isolated from twentyfour animals. Macrophages or neutrophils were cultured in vitro for 3 or 24 h with or without various vitamin E derivatives: free a-tocopherol (a-T), a-tocopheryl acetate (a-TA), or a-tocopheryl succinate (a-TS). Following incubation, cells were stimulated with 80 mM-PMA. Total cell-associated u-PA, membrane-bound u-PA and free u-PA binding sites were determined before and after stimulation with PMA. Results showed that none of the vitamin E derivatives had any effect (P.0·05) on the u-PA system of resting monocyte -macrophages or neutrophils. In contrast, a-TS, but not a-TA or a-T, increased (P,0·01) total cell-associated u-PA and membrane-bound u-PA of PMA-stimulated macrophages and neutrophils. a-TS had no effect (P. 0·05) on total u-PA and membrane-bound u-PA activities of macrophages and neutrophils cultured in the presence of 4-phorbol 12,13 didecanoate, a phorbol ester that does not activate protein kinase (PK) C. Addition of H7 (1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride), which is a potent inhibitor of both PK A and C, completely abolished the effect of a-TS on total cell-associated u-PA and membrane-bound u-PA of PMA-activated macrophages and neutrophils. Addition of HA1004 (N-(2-quanidinoethyl)-5-isoquinoline sulfonamide hydrochloride), which is a potent PK A but a weak PK C inhibitor, had no effect (P.0·05) on total cell-associated u-PA and membrane-bound u-PA of PMA-activated macrophages and neutrophils cultured in the presence of a-TS. Thus, PK C modulates the effect of a-TS on the u-PA system of ovine macrophages and neutrophils.

This study was conducted to evaluate the effects of single and combined deficiencies of selenium and iodine on selenoenzyme activities in sheep. Twenty-four male lambs were assigned to one of four semisynthetic diets: combined deficient A (Se-I), Se-deficient B (Se-I+), I-deficient C (Se+I-), and basal diet D (Se+I+). Thyroid hormones (T3, T4), thyroid stimulating hormone (TSH), and inorganic iodine (PII) were determined in plasma. Selenium and glutathione peroxidase activity (GSH-Px) were determined in erythrocytes, and tissue samples, including the thyroid, liver, kidney, and brain, were taken for selenoenzyme analysis. Plasma T3, T4, and TSH concentrations were similar in all groups. Type I deiodinase (ID-I) activity in liver and kidney remained unchanged in Se or I deficiency. In contrast, hepatic ID-I activity was increased by 70% in combined Se-I deficiency. Thyroidal cystolic GSHPx (c-GSH-Px) and phospholipid GSH-Px (ph-GSH-Px) activities remained constant in both Se-deficient groups, whereas thyroidal c-GSH-Px activity increased (57%) in I deficiency. Type II deiodinase (ID-II) activity was not detectable in the cerebrum and cerebellum, whereas cerebellum Type III deiodinase (ID-III) activity was decreased in I deficiency and combined Se-I deficiencies. The results of the present study support a sensitive interaction between Se and I deficiencies in sheep thyroid and brain. Furthermore, the lack of thyroidal ID-I activity, the preservation of the thyroidal antioxidant enzymes, and the increases in hepatic ID-I indicate that a compensatory mechanism(s) works toward retaining plasma T3 levels, mostly by de novo synthesis of T3 and peripheral deiodination of T4 in Se- and I-deficient sheep.

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1. Effects of dietary conjugated linoleic acid (CLA) on various functional properties of macrophages and heterophils in the laying hen were determined. 2. Seventy two 28-week-old-ISA brown hens were randomly assigned to one of two experimental groups and were fed diets containing 0 or 1% CLA for a total period of 18 weeks. Blood samples were collected from 6 hens per diet group every 3 weeks and macrophages and heterophils were isolated. The following variables were determined in resting and phorbol myristate acetate-activated (65 microM) macrophages and heterophils: total cell-associated urokinase plasminogen activator (u-PA), membrane-bound u-PA, free u-PA binding sites and superoxide production. 3. There were no significant differences between diet groups throughout the whole experimental period in total cell-associated u-PA, membrane-bound u-PA, free u-PA binding sites and superoxide production by resting macrophages and heterophils. 4. Activated heterophils and macrophages isolated from hens fed the CLA-supplemented diet had higher membrane-bound u-PA activity compared with the corresponding values for activated heterophils and macrophages obtained from hens fed the basal diet. These differences were significant for heterophils during weeks 6, 12, 15 and 18 and for macrophages during weeks 6, 9 and 12 of the experiment. 5. Macrophages and heterophils from hens fed the CLA diet had lower superoxide production compared with the corresponding cells from the control hens on weeks 12, 15 and 18 of the experiment. 6. Dietary CLA modulated certain aspects of the immune system in the laying hen. The increased quantity of u-PA on the membrane of macrophages and heterophils isolated from hens fed the CLA diet may facilitate the ability of these cells to reach the point of a potential inflammation (pro-inflammatory effect). 7. In contrast to the effect on the u-PA system, dietary CLA reduced superoxide production by activated macrophages and heterophils during the second half (last 9 weeks) of the experimental period suggesting that CLA may exert an anti-inflammatory effect in the laying hen.