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      Efecto diferencial de la intoxicación crónica por aflatoxina B1 en el crecimiento y en la incidencia de lesiones hepáticas en truchas diploides y triploides (Oncorhynchus mykiss Translated title: Differential effect of chronic aflatoxin B1 intoxication on the growth performance and incidence of hepatic lesions in triploid and diploid rainbow trout (Oncorhynchus mykiss)

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          Abstract

          El propósito del presente estudio fue comparar el crecimiento y la incidencia de lesiones hepáticas en truchas triploides y diploides tratadas con aflatoxina B1(AFB1). 240 truchas fueron divididas en 4 grupos: DC: truchas diploides alimentadas con ración sin AFB1; TC: truchas triploides alimentadas con ración sin AFB1; DT: truchas tratadas con ración con 80 ppb de AFB1 y TT: truchas triploides alimentadas con ración con 80 ppb de AFB1. Durante doce meses, mensualmente, cinco ejemplares de cada grupo fueron anestesiados y sacrificados. Con posteiroridad a la obtención del peso y medición del tamaño de los pesces, muestras hepáticas fueron fijadas en solución de formalina salina 10% y procesadas para análisis histopatológico. El análisis comparativo del rendimiento en crecimiento indicaron diferencias significativas entre truchas diploides del grupo control y del tratado, sugiriendo que AFB1 afecta el crecimiento de las truchas diploides. En truchas triploides no se observaron diferencias entre pesces del grupo control y los pesces tratados. El análisis histopatológico señaló que truchas triploides son más resistentes a AFB1, ya que ambos grupos tratados presentaron lesiones preneoplásicas, sin embargo, el grupo TT demostró menor incidencia de lesiones e igualmente un desarrollo más lento de las mismas. En cuanto a la ocurrencia de neoplasia, en el grupo DT 4 pesces desarrolaron carcinoma hepatocelular en el último trimestre del experimento, mientras que ningún animal triploide desarrolló lesión neoplásica

          Translated abstract

          Triploid trout has been considered to be more resistant than diploid trout to many diseases and to some adverse aquaculture conditions. Considering the common problems with animal food contamination by aflatoxins, the purpose of this research was to compare the incidence of liver lesions and growth performance in triploid and diploid trout (O. mykiss) exposed to chronic contamination with aflatoxin B1. A total of 240 samples formed 4 groups, diploid and triploid control without aflatoxin in food and diploid and triploid treated with 80 ppb of aflatoxin/Kg of food. Five samples in each group were monthly sacrificed during one year. After the measurement of body weight and length, hepatic samples were obtained and fixed in 10% formalin-saline solution. The histopathological analyses were performed with liver slides stained with hematoxylin and eosin. The comparative analyses of the growth performance showed significant difference between control and treated diploid, suggesting that aflatoxin B1 affects the growing of diploid trout. In triploid groups this aspect was not observed. The histopathological analyses indicated that triploid trout is more resistant to aflatoxin B1, since this group did not present neoplastic lesions. Diploid fishes however, showed 4 samples with neoplastic lesion. The triploid treated group had preneoplastic lesion, but with minor incidence and slower progression than diploid trout

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          Mycotoxins: their implications for human and animal health.

          Mycotoxins contaminate various feed and food commodities, due to the global occurrence of toxinogenic molds. They exert adverse health effects in human and animals. The nature of these toxic effects varies depending on the chemical structure of the toxin. The degree of these adverse effects is not only determined by the toxin concentration present in foods and feeds, but also by the time of exposure. Whilst in animals, next to acute intoxication, losses in productivity, reduced weight gain and immunosuppression are considered as most important feature of mycotoxicoses, genotoxic effects and the involvement of certain mycotoxins such as aflatoxin, ochratoxins and fumonisins in the etiology of human cancers have obtained particular attention. This implies that recent research activities concentrate on mechanistic aspects of mycotoxin-induced pathologies, rather than compiling analytical measures of mycotoxin concentrations in food and feeds.
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            Fish models for environmental carcinogenesis: the rainbow trout.

            Progress over the past 30 years has revealed many strengths of the rainbow trout as an alternative model for environmental carcinogenesis research. These include low rearing costs, an early life-stage ultrasensitive bioassay, sensitivity to many classes of carcinogen, a well-described tumor pathology, responsiveness to tumor promoters and inhibitors, and a mechanistically informative nonmammalian comparative status. Low-cost husbandry, for example, has permitted statistically challenging tumor study designs with up to 10,000 trout to investigate the quantitative interrelationships among carcinogen dose, anticarcinogen dose, DNA adduct formation, and final tumor outcome. The basic elements of the trout carcinogen bioassay include multiple exposure routes, carcinogen response, husbandry requirements, and pathology. The principal known neoplasms occur in liver (mixed hepatocellular/cholangiocellular adenoma and carcinoma, hepatocellular carcinoma), kidney (nephroblastoma), swim bladder (adenopapilloma), and stomach (adenopapilloma). Trout possess a complex but incompletely characterized array of cytochromes P450, transferases, and other enzymic systems for phase I and phase II procarcinogen metabolism. In general, trout exhibit only limited capacity for DNA repair, especially for removal of bulky DNA adducts. This factor, together with a high capacity for P450 bioactivation and negligible glutathione transferase-mediated detoxication of the epoxide, accounts for the exceptional sensitivity of trout to aflatoxin B1 carcinogenesis. At the gene level, all trout tumors except nephroblastoma exhibit variable and often high incidences of oncogenic Ki-ras gene mutations. Mutations in the trout p53 tumor suppressor gene have yet to be described. There are many aspects of the trout model, especially the lack of complete organ homology, that limit its application as a surrogate for human cancer research. Within these limitations, however, it is apparent that trout and other fish models can serve as highly useful adjuncts to conventional rodent models in the study of environmental carcinogenesis and its modulation. For some problems, fish models can provide wholly unique approaches. Images Figure 1. Figure 2. Figure 3. Figure 4. Figure 5. Figure 6. Figure 7. Figure 8. Figure 9. Figure 10. Figure 11. Figure 12.
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              Ploidy manipulation and performance

                Author and article information

                Journal
                amv
                Archivos de medicina veterinaria
                Arch. med. vet.
                Facultad de Ciencias Veterinarias, Universidad Austral de Chile (Valdivia, , Chile )
                0301-732X
                2002
                : 34
                : 2
                : 253-263
                Affiliations
                [03] São Paulo orgnameHealth Secretary from the State of São Paulo orgdiv1Unit of Biological Chemistry, Adolfo Lutz Brazil
                [04] São Paulo orgnameUniversity of São Paulo orgdiv1Faculty of Zootechny and Food Engineering Brazil
                [02] São Paulo orgnameAgriculture Secretary from the State of São Paulo orgdiv1Fishery Institute Brazil
                [01] São Paulo SP orgnameState University of Campinas orgdiv1Institute of Biology orgdiv2Department of Histology and Embryology Brazil aranas@ 123456obelix.unicamp.br
                Article
                S0301-732X2002000200011 S0301-732X(02)03400211
                789011da-0ba8-444e-a3fc-6806174110a6

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

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                Figures: 0, Tables: 0, Equations: 0, References: 28, Pages: 11
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                SciELO Chile

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                ARTICULOS ORIGINALES

                triploidia,triploidy,Rainbow trout,hepatocarcinogenesis,aflatoxina,Trucha arco iris,aflatoxin

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