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

1 st WorkshopXIII International Feed Technology SymposiumPrimary toxic effects of aflatoxin are formed at the level of interaction with geneticmaterial. Molecule penetrates the cell and its nucleus, and enters between the base pairsof DNA. Create errors in the transcription of DNA, which greatly slows down theprocess of transferring information, a consequence is the inhibition of protein synthesisand synthesis of "wrong" protein. Immunosuppressive effects of aflatoxin are alsoproven in chickens and turkeys, as well as in some laboratory animals [12].Aflatoxins are very toxic compounds, for most animal species. The relative toxicity(LD50) for the most sensitive ducks and turkeys is 0,3-0,6 mg/kg BW, pigs 0.6 mg/kgBW and ruminants 0.2 mg/kg BW, while most resistant are chickens 6,5-16,5 mg/kg BW[12].The clinical signs of acute aflatoxicoses are characterised by depression, anorexia,icterus and hemorrhages. Steatorhea is a common finding, and hemorrhages in manyparts of the body of pigs, in lactating animals milk production reduction to the completecessation, and mortality in birds for 7-14 days in most opistotonusu and legs extendedbackwards. In broilers this disorder [22], manifests as retarded growth and lower feedconversion (0.25 kg/kg), impaired imunogenesis (0.6 mg/kg) or egzitus (about 1 mg/kg).In laying hens the most striking changes are in some biochemical parameters, anddecrease of egg production and weight. In chronic aflatoxicoses clinical picture isatypical and is manifested by reduction of feed consumption, increase conversions,decrease body weight, milk and egg production, as well as the significantimmunosuppresion. The consequences are carcinogenic, mutagen, embriotoxic andteratogenic effects.Pathomorphological changes develop in multiple organs, and one of the indicators ofaflatoxin intoxication is increased relative weight of internal organs. As it belongs tohepatotoxic group of mycotoxins, the most common and the most visible changes areobserved in the liver, in the form of discoloration, necrosis, hemorrhages, fattyinfiltration and atrophy. Also hemorrhages and necrosis are present along the entireintestinal tract with proliferation of biliary channels. Aflatoxin B1 causes the kidneysnefroses, and the toxin amount in feed greater then 0.2 ppm causes testicular atrophy,interruptions in germinative epithelium and spermatogenesis termination, as well asslower development of the ovaries with reduced relative weight and expressed folicularatresis [24].OCHRATOXINOchratoxin is synthesized by storage fungi of the genus Aspergillus (A. alutaceus, A.sulphureus, A. melleus, A. alliaceus) and Penicillium (P. viridicatum, P. verrucosum, P.cyclopium, P. commune) in conditions of humidity higher then 16%, while the optimaltime for the creation of toxin is 7-14 days. Maximum production occurs at temperatures20-25 0 C, but it is possible in the range from 2 to 31 0 C.Ochratoxin is mostly resorbed in the front parties of the digestive tract and viabloodstream it reaches the kidneys and liver, primarily, but to a lesser extent to themuscles also where it deposites. Excretion is mainly carried out through the urine andfeces, while the elimination by milk is minimal. Excretion by eggs is also noted [19].The mechanism of action of ochratoxin is based primarily on the effect of the enzymesinvolved in the metabolism of phenylalanine and mitochondria function [28]. The98