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pubmed-article:1830044pubmed:dateCreated1991-8-20lld:pubmed
pubmed-article:1830044pubmed:abstractTextThe effects of dietary restriction of vitamin E (Vit E) and selenium (Se) on lymphocyte proliferation, natural killer (NK) cell activity, antibody-dependent cell-mediated cytotoxicity (ADCC), and on burst respiratory response of stimulated granulocytes as measured by chemiluminescence (CL) were studied in pigs. Six male weanling pigs were maintained for 25 d on a torula yeast-based diet containing no measurable amount of alpha-tocopherol and less than .02 mg of Se per kilogram of feed. Six others received the same basal diet supplemented with 33 IU of DL-alpha-tocopheryl acetate and .2 mg of Se per kilogram of feed. All pigs were inoculated with Salmonella typhisuis on d 21 of the feeding period and killed on d 25. Tests to measure cellular immune functions were performed on cells isolated from blood samples taken on d 21 and 25. After 21 d of feeding, lymphocyte blastogenesis responses to phytohemagglutinin, concanavalin A, and pokeweed mitogen in pigs fed the Vit E- and Se-deficient diet were normal compared with the response in pigs fed the supplemented diet. Moreover, the cytotoxic activity of NK cells, the ADCC response, and the CL response of granulocytes were not affected. After 25 d, a marked suppression of lymphocyte response to mitogens occurred in pigs fed the Vit E- and Se-deficient diet when the cells were cultured in the presence of autologous serum. When fetal bovine serum replaced autologous serum in the cultures, no suppression was observed. No effect on NK activity and ADCC was observed, whereas the CL peak response of granulocytes tended to be higher in pigs fed the deficient diet.(ABSTRACT TRUNCATED AT 250 WORDS)lld:pubmed
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pubmed-article:1830044pubmed:pagination1575-82lld:pubmed
pubmed-article:1830044pubmed:dateRevised2003-11-14lld:pubmed
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pubmed-article:1830044pubmed:year1991lld:pubmed
pubmed-article:1830044pubmed:articleTitleCellular immune responses in pigs fed a vitamin E- and selenium-deficient diet.lld:pubmed
pubmed-article:1830044pubmed:affiliationUniversity of Wisconsin, Madison 53706.lld:pubmed
pubmed-article:1830044pubmed:publicationTypeJournal Articlelld:pubmed