Toxic effects to mink of moniliformin extracted from Fusarium fujikuroi culture material.

Acute and subacute effects of i.p. exposure to moniliformin in mink (Mustela vison) were investigated. Moniliformin was extracted from Fusarium fujikuroi culture material containing 9,174 ppm moniliformin. An acute LD50 between 2.2 and 2.8 mg moniliformin/kg bw was determined for 9-mo-old female mink. Subacute exposure to 1.5 to 3.2 mg total moniliformin/kg bw resulted in dilated (right side) hearts rounded in appearance. Statistical differences observed in serum chloride and albumin, amylase activities, spun packed-cell volumes, red blood cell counts, hemoglobin concentrations, and hematocrit values between control and moniliformin-dosed mink were considered biologically insignificant because values were within ranges reported for normal mink. Electron microscopic examination of the right ventricular free heart wall of mink receiving acute or subacute doses of moniliformin revealed ultrastructural damage to myofibers, mitochondria, nuclei, Z- and M-lines and sarcoplasmic reticula, and increased extracellular collagen deposition. These results showed that mink are among the more sensitive mammals to moniliformin and that this mycotoxin specifically targets and damages the hearts of mink.

Effects of supplemental dietary sodium chloride and restricted drinking water on mink.

Thirty-six male mink were fed diets that contained 0, 1, 2 or 4% supplemental salt (sodium chloride) and were given drinking water ad libitum for 7 d. Three mink on each diet were then placed on ad libitum, 50% ad libitum or 25% ad libitum drinking water for the next 14 d. Ad libitum water consumption was directly proportional to the salt content of the diets. Feed consumption was inversely related to the level of dietary salt, although water restriction had a greater effect in reducing feed consumption than did the supplemental salt. The clinical signs of salt toxicity-water restriction observed were increased thirst, mild dehydration, decreased feed consumption, decreased body weight, rough coat, crusty nose and eyes, irritability in the early stage, and lethargy in the later stages. In general, serum and urinary sodium and chloride ion concentrations increased with increasing dietary salt concentrations. Expressed as a percent of brain weight, liver, spleen, kidney and heart weights of mink fed supplemental salt were less than the control weights. Adrenal gland weights increased in response to water restriction. Brain sodium concentrations were not affected by salt supplementation when drinking water was provided ad libitum. However, restricting drinking water generally resulted in increased brain sodium concentrations. Mild to moderate micro- or macrovesicular vacuolar changes were observed in the livers of some mink fed each level of dietary salt, but were especially prominent in the mink restricted in drinking water.

Feeding supplemental iodine to adult mink; effect on thyroid hormones in adult and offspring.

We fed adult mink diets containing supplemental iodine, from 0 to 320 ppm, for one or seven months prior to breeding. Blood samples collected from the adults and their offspring (kits) at 4 wk post-partum were assayed for total thyroxine (T4), triiodothyronine (T3), reverse T3 (rT3), and T4-binding indices. As expected T4 concentrations of the adult and kit mink varied inversely with the level of supplemental iodine. In addition, T3 and rT3 concentrations decreased gradually in kits from the long-term experiment in response to the increased dietary iodine of the dams. T3 concentrations of kits from dams fed iodine short-term decreased markedly while rT3 concentrations were elevated greatly in response to increased dietary iodine of the dam. These decreases in hormone levels are due to serum iodine blocking the thyroid uptake of iodine and subsequent decrease of hormone synthesis. Excess iodine may also block the effect of thyroid stimulating hormone. The T4-binding indices of the adults, in general, were depressed, while the T4-binding indices of the kits were more variable. These effects are probably due to fluctuations in thyroglobulin.

Toleration of high concentrations of dietary zinc by mink.

Adult and kit male and female natural dark ranch mink (Mustela vison) were fed a conventional diet supplemented with 0, 500, 1,000, or 1,500 ppm zinc, as ZnSO4.7H2O, for 144 days. No marked adverse effects were observed in feed consumption, body weight gains, hematologic parameters, fur quality, or survival. Zinc concentrations in liver, kidney, and pancreas of the mink increased in direct proportion to the zinc content of the diet. Histopathologic examination of the livers, kidneys, and pancreata revealed no lesions indicative of zinc toxicosis. The results indicate that mink can tolerate at least 1,500 ppm dietary zinc, as ZnSO4.7H2O, for several months without apparent adverse effects.

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.

Feeding supplemental iodine to mink: reproductive and histopathologic effects.

Adult mink were fed various concentrations of supplemental iodine, ranging from 10 to 320 ppm, for 1 or 7 mo before breeding. Long-term, low-level (10-20 ppm) iodine supplementation was beneficial for both reproduction and lactation. Supplemental iodine in excess of 80 ppm, however, resulted in a reduction in the number of females that whelped, a decrease in litter size, and an increase in kit mortality. Thyroid glands of kits whelped and nursed by dams fed more than 20 ppm supplemental iodine, both short-term and long-term, showed hypertrophy marked by follicular cell hyperplasia and a decreased amount of colloid. Similar histopathologic lesions were observed in the thyroids of adults that received 80 ppm or more supplemental iodine; also observed were numerous lesions in the gallbladder.

Effects of supplemental dietary copper on growth, reproductive performance and kit survival of standard dark mink and the acute toxicity of copper to mink.

Natural dark mink kit were fed a diet supplemented with 0, 25, 50, 100 or 200 ppm Cu from CuSO4 . 5H2O for 153 or 357 d. The shorter term Cu supplementation had no significant beneficial or adverse effects on mink body weight gains or hemoglobin or hematocrit concentrations, although plasma Cu concentrations were slightly elevated in the mink fed added Cu. Liver Cu concentrations were significantly increased only in the mink fed 200 ppm Cu. Liver Zn and Fe concentrations were not affected by the added Cu. Darker fur was observed in pelted males fed the higher levels of Cu. The reproductive performance of mink on the longer term Cu supplementation was not adversely affected, although greater kit mortality and reduced "litter mass" were a result of the higher Cu concentrations. The acute (21-d) ip LD50 concentrations of Cu sulfate and Cu acetate in adult mink were 7.5 and 5.0 mg/kg, respectively.