White Leghorn chicken (Gallus domesticus) eggswere injected prior to incubation with one of four concentrations (0.001,0.01, 0.1, and 1.0 egg-equivalent) of an extract derived from 1,000double-crested cormorant (Phalacrocorax auritus) eggs collected atSpider Island adjacent to Green Bay in Lake Michigan. One egg-equivalentcorresponded to the concentration of contaminants present in an averagecormorant egg. This was approximately 322 pg toxic equivalents (TEQs)/g, wwegg with polychlorinatedbiphenyl congener 126(3,3',4,4',5-pentachlorobiphenyl) accounting for over 70% of the TEQs.Injection of 1.0 egg-equivalent resulted in 77% mortality at hatch.The incidence of developmental abnormalities (structural defects or edema)was not affected by injection of the extract. Body weight gain of chicks wasreduced in the 1.0 egg-equivalent dose group in the first, second, and thirdweek's post-hatch. Relative brain weights were greater and relativebursa weights were less in the 1.0 egg-equivalent dose group than in thevehicle control at three weeks of age. There were no significant differencesin the relative weights of the heart, liver, spleen, testes, or comb amongtreated and control birds.
Adult female mink (Mustela vison) were fed a diet that contained Fusarium moniliforme culture material that provided dietary concentrations of 89 ppm fumonisin B1, 21 ppm fumonisin B2, and 8 ppm fumonisin B3 for 87 days. During the trial, there was mild lethargy in the mink fed fumonisins, but no other clinical signs or differences in feed consumption (measured during the first two weeks), body weights, or survivability were observed between the fumonisin-treated and control mink. Several hematologic parameters (mean corpuscular hemoglobin concentration, plasma total solids, and lymphocyte concentration) and serum chemical concentrations (globulin, phosphorus, potassium, blood urea nitrogen, creatinine, bilirubin, and cholesterol) and activities (alkaline phosphatase, alanine aminotransferase, amylase, and aspartate aminotransferase) were greater in the mink fed fumonisins than in the controls. Serum albumin/globulin and sodium/potassium ratios and chloride concentrations were lower in the fumonisin-fed mink than in the controls. The concentrations of free sphinganine and the ratio of free sphinganine to free sphingosine in the liver and kidneys of the fumonisin-treated mink were greater than in the control mink. No histopathologic alterations were associated with fumonisin treatment. These results indicate that long-term dietary exposure to F. moniliforme culture material containing 118 ppm total fumonisins is not lethal to adult mink, but can produce adverse physiological effects in the animals.
Rats were fed polybrominated biphenyls (PBBs) at 0.1 to 100.0 ppm for 14 d and then treated to hasten the removal of PBBs with 0, 5, or 10% mineral oil (MO) and/or 0, 15, 30, or 45% feed restriction (FR) for 21 d. PBB body burdens were determined at d 14 and expressed on a log-log basis by Y = 0.91X + 2.179 (r2 = 0.974), where X = log of PBB concentration in diet (ppm) and Y = log of PBB body burden (micrograms). After 21 d withdrawal, body burdens were expressed by the equation Y = 0.787X + 2.218 (r2 = 0.95). The most effective withdrawal treatment was 10% MO + 45% FR producing a reduction of body burdens inversely related to prior body burdens (69% at 0.1 ppm to 23% at 100 ppm). Body weights and fat content were significantly (p less than or equal to .05) reduced by feed restriction, with fat content only 39% of controls at 21 d off. Mortality averaged 0, 13.6, and 35.8% for rats fed 0, 5, or 10% MO, and 25, 15, 8.6, and 3.7% for rats feed restricted at 0, 15, 30, and 45%, respectively. Histopathology of the dead and moribund rats indicated that the clinical signs were not characteristic of PBB toxicity. In a second experiment, safflower oil at 3.5% or excess vitamins prevented the mortality and clinical signs associated with MO during withdrawal from 100 ppm PBBs. Based on these data and those in the literature, PBBs interfere with vitamin utilization.
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