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Administration of ochratoxin A and T-2 toxin to growing swine.
1994
Harvey R.B. | Kubena L.F. | Elissalde M.H. | Rottinghaus G.E. | Corrier D.E.
Effects of dietary ochratoxin A (OA) and T-2 toxin, fed singly and in combination, were evaluated in growing crossbred pigs. Thirty-six barrows (3 replicates of 3 for each of 4 treatment groups, mean body weight, 18.0 kg) were fed: 0 mg of OA and 0 mg of T-2/kg of feed (control); 2.5 mg of OA/kg of feed; 8.0 mg of T-2/kg of feed; or 2.5 mg of OA plus 8.0 mg of T-2/kg of feed for 30 days. Production performance, serum biochemical, hematologic, immunologic, and pathologic evaluations were made. Body weight and body weight gain were decreased by all toxin treatments, but the combination toxin treatment reduced weight gain more than did either of the toxins administered singly and could be considered additive. Liver weight was decreased by combination treatment, whereas kidney weight was increased by OA treatment. Ochratoxin decreased serum cholesterol, inorganic phosphorus, and alkaline phosphatase values; reduced mean cell volume, hemoglobin concentration, and macrophage phagocytosis; and increased creatinine and total protein values. Consumption of T-2 toxin reduced hemoglobin and serum alkaline phosphatase values. The combination treatment decreased serum cholesterol, gamma-glutamyltransferase, alkaline phosphatase, mean cell volume, hematocrit, and hemoglobin values, as well as lymphoblastogenesis and phagocytosis, and increased serum nine concentration. We concluded that OA and T-2, singly or in combination, can affect clinical performance, serum biochemical, hematologic, and immunologic values, and organ weights of growing barrows. Although some analytes were affected more by the combination than by either toxin alone, the interactions could best be described as additive, not synergistic.
Mostrar más [+] Menos [-]Studies on toxicity of ochratoxin a to chromosomes of tumor cell-line.
1989
Yoon W.J. | Roh M.H. | Kim K.R.
This study was performed to investigate the toxicity of ochratoxin A (OA) to the chromosomes of K562 tumor cell-line in vitro. Chromosomes of K562 tumor cell-line resulted in pseudotriploidy on the control group. Chromosomes of K562 tumor cell-line treated with OA resulted in heteroploidy compared with the control group. The mean number of chromosomes in the karyotype of the control group (60) were 7 in the A group, 5 in the B group, 20 in the C+X group, 7 in the D group, 9 in the E group, 6 in the F group, and 6 in the G+Y group respectively. Treating with 0.7 micro M OA, the number of chromosomes were increased one in E and F group, two in G+Y group compared with control group. In treated with 1.5 micro M OA, the increasing number of chromosome was one in E and F group. In treated with 3 micro M OA, E and F group was increased one and G+Y group were increased two chromosome in G+Y group was decreased one. K562 tumor cell line treated with OA showed Philadelphia-Chromosome in the long arm of the G group karyotype chromosome. The rate of chromosome aberration in K562 tumor cell-line treated with OA was 77 % in 0.7 micro M OA group, 71 % in 1.5 micro M OA group, 82 % in 3 micro M OA group and 94 % in 6 micro M OA group respectively. The rate of chromosome aberration of K562 tumor cell-line treated with OA was high in the high dose level of OA, and chromosome aberration of K562 tumor cell-line treated with OA showed deletion, minute, dicentric-chromosome and translocation in the long arm of the C-group karyotype. As a result of this study, the toxicity of OA showed deletion, minute, dicentric-chromosome and translocation in the long arm of the C-group karyotype, and then, the toxicity of OA resulted in the damage to RNA and protein synthesis in K562 tumor cell-line, and the C-group karyotype of K562 tumor cell-line was target of the toxicity of OA.
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