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

1 st WorkshopXIII International Feed Technology Symposiumbeen registered and described a single case of fumonisintoxicoses in our country, butpresence of these types of Fusarium fungus in our country, and the isolation offumonisin B1 from several samples of corn and soybean meal, it is considered that theoccurrence of this mycotoxicoses in our area is also possible [16].DEOXYNIVALENOLDeoxynivalenol (DON), often called the vomitoxin, is mainly isolated from corn andother cereals, oil meals, hay and silage, and produced by fungi genus Fusarium (F.graminearum, F. semitectum, F. Nivala and F. poae). For his presence in feed for pigsthe phenomenon of feed refusal, diarrhea, vomiting, reproductive disorders and mortalityare linked [35]. DON in cattle does not cause serious health disorders due to theactivities of rumen microflora, which transformes it into a less toxic metabolites, whichthen is largely excreted from the body. Deoxynivalenol is often the cause of poor feedconsumption [34] and reduced milk production in dairy cows. At the beginning oflactation cows with high milk production, which are under greater stress and lowerimmunity, and cattle in nutrition deficiency with the weaker degradation of mycotoxinsin the rumen, are more sensitive. Fattening cattle and sheep tolerate higherconcentrations of deoxynivalenol in feed, without affecting consumption, growth andfeed conversion [2, 36].T-2 TOXINT-2 toxin occurs as a toxic product of the fungal genus Fusarium (F. tricinctum, F.roseum, F. poae, F. sporotrichioides) that synthesize it at lower temperatures (2-40 0 C),while at temperatures above 32 0 C they lose this ability.After ingestion T-2 toxin is rapidly resorbed in front parties of the digestive tract, andalready after 1 h reaches its maximum concentration in blood. Then follows the slowerphase and the distribution of T-2 toxin and its metabolites in some tissues, while after 3-4 h the highest amount can be found in the liver, kidneys, stomach and bile, and in themuscle and skin reaches a maximum after 12 h. After 24 h the highest concentration ofT-2 toxin in the excreting organs and in the bile duct, liver, kidneys and intestines.Enterohepatic recirculation delay excretion and increases toxicity (phenomenon ofdelayed effects). Elimination of T-2 toxin and metabolites occurs via the urine during thefirst 24 hours, and then the remaining part is excreted via feces. Ingested T-2 toxin is leftas a deposit significantly in any organ, and the residues are effectively eliminated duringthe few days after the termination of consumption of contaminated feed. During theconsumption of contaminated feed, T-2 toxin is excreted by eggs, and his concentrationis higher in albumen than in yolk (0.04 vs. 0.13%). During the long-term intoxication,eggs excrete about 0.1% of ingested toxin [27].T-2 toxin inhibits the replication of DNA, and causes changes in DNA that have nonreversalcharacter, but nevertheless T-2 toxin is considered, with prolonged action, thatcan induce mutagen, teratogenic and carcinogenic effects. Many trichotecens inhibitprotein synthesis by blocking elongation of polypeptide chain at the position of peptidiltransferasein polysome subunits 60S. It was also noticed the possibility of irreversibleinhibition of initiation of protein synthesis that leads to decay of polysomes. This toxin95