10.07.2015 Views

Effects of dietary n-3 polyunsaturated fatty acids and ... - FINS

Effects of dietary n-3 polyunsaturated fatty acids and ... - FINS

Effects of dietary n-3 polyunsaturated fatty acids and ... - FINS

SHOW MORE
SHOW LESS

Create successful ePaper yourself

Turn your PDF publications into a flip-book with our unique Google optimized e-Paper software.

1 st WorkshopXIII International Feed Technology SymposiumZearalenone <strong>and</strong> its metabolites have anabolic effects, similar to estrogen <strong>and</strong>foliculostimulative hormone. Biological activity can be explained by competition with17- -estradiol for specific binding sites on estrogen receptors <strong>and</strong> interference withenzymes involved in metabolism <strong>of</strong> steroides. The mechanism <strong>of</strong> action is based onbinding to estrogenic receptors in the cytosol, <strong>and</strong> the mycotoxin-receptor complex istransported into the cell nucleus. F-2 demonstrates the effects <strong>of</strong> toxins in all themetabolic processes affected by estrogen hormones [18], but usually in the genitalorgans <strong>and</strong> in the process <strong>of</strong> reproduction. The consequence is, primarily, prematuresexual development in immature female <strong>and</strong> inhibition <strong>of</strong> normal development <strong>of</strong> thetestecles in males.Zearalenone is characterized by slightly less toxicity, compared to other metabolites <strong>of</strong>Fusarium fungus. Toxic effect in different animal species, or the relative toxicity (LD50)ranges from 1-10 mg/kg BW zearalenone <strong>and</strong> therefore belongs to a very toxicmycotoxins. Pigs are more sensitive to its effects [6] then other animal species, such asruminants <strong>and</strong> poultry, especially chickens. F-2 toxin has cytotoxic <strong>and</strong> genotoxic effects[4].The type <strong>and</strong> intensity <strong>of</strong> symptoms <strong>of</strong> zearalenontoxicoses depends on the animalspecies, age <strong>and</strong> gender. In the clinical picture is dominant estrogen syndrome which ismanifested by edema <strong>and</strong> vulvar hyperemia, with slightly muculagineus vaginaldischarge. In severe cases, prolapsus <strong>of</strong> vagina <strong>and</strong> rectum could be seen. F-2 toxin atlow doses increases the size <strong>of</strong> the milk gl<strong>and</strong>s <strong>and</strong> reproductive organs <strong>and</strong>/or causesearly maturation. In higher doses, negatively affects the conception, ovulation,implantation, fetal development <strong>and</strong> vitality <strong>of</strong> newborn animals. In addition, in theclinical picture also may occur diarrhea, vomiting, feed refusal, loss <strong>of</strong> weight <strong>and</strong>hemorrhages. Characteristic pathomorphologic changes in the external genital organs in<strong>of</strong>ten are observed in the form <strong>of</strong> edema <strong>and</strong> hyperemia [20].AFLATOXINAflatoxins are a mixture <strong>of</strong> similar chemical compounds labeled by fluorescing coloursas B (blue), which are significantly more toxic, <strong>and</strong> G (green). They are products <strong>of</strong>secondary metabolism <strong>of</strong> molds Aspergillus flavus <strong>and</strong> Aspergillus parasiticus, althoughthere are opinions that other strains <strong>and</strong> species also have the ability <strong>of</strong> synthesis <strong>of</strong> thesetoxins in the traces. Aspergillus fungi are capable <strong>of</strong> growth <strong>and</strong> sporulation in thetemperature range 6-54 0 C, while the optimal are temperature 30-35 0 C, minimum <strong>of</strong> 0.78aw for growth <strong>and</strong> optimal pH is 5.5.Ingested aflatoxin is effectively resorbed in the digestive tract <strong>and</strong> reaches thebloodstream for 30 minutes <strong>and</strong> the hepatocytes for 1 hour where its biotransformationsstarts. It is believed that among the metabolites aflatoxicol is the most mutagen agentthat causes carcinogenic changes in the liver. Excretion is mostly done via bile <strong>and</strong> urine<strong>and</strong> to a lesser extent by milk (aflatoxins M). After 24 hours in the body remains 20-30%<strong>of</strong> the entered aflatoxin. The biological half-time decay is 72-96h, <strong>and</strong> 7 days after use <strong>of</strong>contaminated feed aflatoxin residues <strong>and</strong> its metabolites were found only in eggs <strong>and</strong>milk. Aflatoxin tends to be deposited in all s<strong>of</strong>t tissues <strong>and</strong> fat depots, mostly in the liver<strong>and</strong> kidneys. Detection <strong>of</strong> residues is relatively difficult <strong>and</strong> possible only for the originalform <strong>of</strong> toxin <strong>and</strong> its metabolite M1 [24].97

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!