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Department of Animal Science and Center for Environmental Toxicology, Michigan State University, East Lansing, MI 48824-1225
Dietary exposure to 1000 ppm of supplemental Zn did not result in grossly observable Zn toxicity or Zn-induced Cu deficiency in adult mink. These same concentrations did, however, produce achromatrichia, alopecia, lymphopenia and a reduced rate of growth in the offspring produced by the Zn-treated females. These mink kits also exhibited profound immunosuppression. The in vitro blastogenic response of peripheral blood lymphocytes to concanavalin A was significantly (P < 0.001) lower in kits born to Zn-treated dams than the response of those born to control dams. The depressed immunoresponsiveness was not a permanent defect since a normal lymphocyte response was seen approximately 14 weeks after weaning and being placed on an unsupplemented basal diet. The impaired lymphocyte reactivity is believed to be the result of altered DNA synthesis in these cells and/or an inhibition of macrophage functions necessary for normal response to the mitogen concanavalin A.
KEY WORDS: zinc immunosuppression mink lymphocyte blastogenesis concanavalin A
1 Supported in part by the Mink Farmer's Research Foundation, Thiensville, WI and published with the approval of the Michigan Agricultural Experiment Station as Journal Article Number 10842.
Manuscript received 9 May 1983.
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