Proliferation of periodontal squamous epithelium in mink fed 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

The maxilla and mandible from 2 adult female mink fed 5.0 ppb 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for 6 mo were grossly unremarkable, but histologically had nests of squamous epithelium within the periodontal ligament. There was osteolysis of the adjacent alveolar bone.

Effects of dietary exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin in adult female mink (Mustela vison).

Adult female mink were fed diets supplemented with 0, 0.001, 0.01, 0.1, 1, 10, or 100 ppb 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for up to 125 days. There was a dose-dependent decrease in feed consumption and body weights indicative of the "wasting syndrome" previously reported for mink and other species exposed to chlorinated hydrocarbon compounds. Mortality reached 12.5, 62.5, and 100% by day 28 in the 1-, 10-, and 100-ppb groups, respectively, and by day 125, mortality increased to 62.5 and 100% in the 1- and 10-ppb groups, respectively. Adrenal gland weights were significantly greater in the three highest dose groups compared to the control group. The percentage of band neutrophils was also significantly greater in the TCDD-treated groups compared to the control. LC50 (+/- SE) values for 28 and 125 days of dietary exposure to TCDD were calculated to be 4.8 +/- 4.99 ppb and 0.85 +/- 0.64 ppb, respectively. Based on feed consumption of control mink, these LC50 concentrations approximate 0.264 and 0.047 microgram TCDD/kg body weight/day for the 28- and 125-day exposure periods, respectively. These results confirm the sensitivity of mink to TCDD.

Chronic toxicity of dietary fluorine to mink.

Seventy-two 3-mo-old pastel mink were fed diets that contained 0, 33, 60, 108, 194 or 350 ppm supplemental fluorine (F), as NaF, for 382 d to assess its effects on growth, fur quality, reproduction and survivability. The basal diet contained 35 ppm F as fed. No significant differences were observed in body weight gains or fur quality between the controls and any of the F-treated groups (P greater than .05). Some males fed 350 ppm supplemental F for a 4-mo period prior to pelting had weakened frontal, parietal and femoral bones that fractured during the pelting process. The F treatments had no measurable adverse effects on breeding, gestation, whelping or lactation, although only 14% of the kits whelped by females fed 350 ppm F survived to 3 wk of age. The survivability of the adult mink was adversely affected only at 350 ppm supplemental F. At the termination of the study, no differences were observed in hematologic parameters or serum calcium concentrations between the controls and treated mink (P greater than .05), but serum alkaline phosphatase activities were increased (P less than .05) by the two highest dietary F levels. Serum F levels were elevated (P less than .01) only in mink fed 194 and 350 ppm F, and urinary and femoral F concentrations in the treated animals were generally greater (P less than .05; P less than .01) than control values and were closely related with dietary F levels. Femoral ash contents of the 194 and 350 ppm F-treated mink were less than the control values (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of excessive dietary zinc on the intrauterine and postnatal development of mink.

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 less than 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.