Mycotoxins in Feedstuffs

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The association of mycotoxin production and physical damage to grain and drought during grain ripening indicates that Aspergillus spp. During long grain storage, the biochemical activity of grain is much reduced, while invasion of storage fungi and mycotoxin contamination would increase. More data is needed on the biochemistry and pathogenesis of toxigenic fungi to understand and evaluate their genotype.

The germination and viability of maize seeds could be affected by attack of Aspergillus and Penicillium species and their fungal infestation have been found to be different among maize genotypes Similarly, genotypes of peanut and biochemical properties of its seed such as tannin content 11 , thin pericarp 12 , small amount of cuticular wax 13 and chemical composition of the pericarps and embryos 14 have been shown to inhibit fungal invasion by A.

Recently, antifungal enzymes, chitinase 15 and B-1, 3-glucanase 16 , found in a number of plant seeds, may act as defense against pathogenic fungi, since chitin and glucan are major polymeric components of many fungal cell walls. Such polysaccharides in fungal cell wall could be enzymically hydrolysed into smaller products resulting the damage or killing of fungal mycelia or spores. The role of these enzymes for genotype evaluation is now being studied.

It is foreseen that seeds rich in such antifungal enzymes likely resist the infestation of fungi. If so, the seeds for breeding would be easily screened out and used a stock one. Even there are many technical problems in searching for the "super" plant against pathogenicity, the development of fungal-resistant plant varieties utilizing genetic resistance to mycotoxin contamination is still possible and encouraged. How to prevent growth and invasion of pathogenic fungi in agricultural commodities is very important in preventing mycotoxin contamination.

The inhibition of fungal growth can be achieved by physical, chemical and biological treatments Contaminated mycotoxins in foods and feeds should be removed, inactivated or detoxified by physical, chemical and biological means depending on the conditions. However, the treatment has its own limitations, since the treated products should be healthsafe from the chemicals used and their essential nutritive value should not be deteriorated.

The following methods are suggested to be applied for effective decontamination of some mycotoxins. Physically, fungi-contaminated seeds can be removed by hand picking or photoelectric detecting machines.

Mycotoxins Definition

The method would consume time and Iabor or expensive. Organic solvents chloroform, acetone, hexane and methanol have been used to extract aflatoxins for agricultural products, but mainly in vegetable oil refining process Ionizing radiation such as gamma-rays can stop growth of food spoilage organisms, including bacteria, molds and yeasts. It also inactivates pathogenic organisms including parasitic worms and insect pests.

It has been reported that gammairradiation M-rad caused reduction of aflatoxin The irradiation, however, could not completely destroy the toxin and its mutagenicity. The treatment combination of gamma irradiation and ammoniation should be therefore attempted for more aflatoxin decontamination. Chemical treatment has been used as the most effective means for the removal of mycotoxins from contaminated commodities.

Mycotoxin prevention and control in foodgrains - Prevention and control of mycotoxins

The method should be sure that the detoxification system is capable of converting the toxin to a nontoxic derivative s without deleterious change in the raw product. Mutagenicity of the treated products should be assessed. The toxicity may be checked by feeding animals including bouts, egg embryos, chicken, ducklings and rats. Many common chemicals have been brought to test the effectiveness in detoxification of aflatoxin. These chemicals include the followings:.

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The chemical reactions of detoxification of aflatoxin are primary addition of the double bond of the furan ring and oxidation involving phenol formation and opening of the lactone ring. In the presence of acid, aflatoxins B.


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Figure 1 Proposed formation of aflatoxin-related reaction products following exposure to ammonia. Figure 3 Comparison of reduction of AFB1 content in different treatment periods and their mutagenicities.

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Other mycotoxins which are like aflatoxin and have a lactone grouping in the molecule can be similarly destroyed by alkaline condition using ammonia, sodium hydroxide and sodium bicarbonate. These toxins are patulin, penicillin acid, citreoviridin, citrinin, cyclochlorotin, ochratoxin A, rubratoxin, trichothecenes and zearalenone.

Certain conditions such as moisture content, heat, ultraviolet or gamma irradiation, sunlight and pressure at different treatment-periods have been simultaneously combined with the chemicals for the enhancement of detoxification. Inactivation methods can be achieved by mixing, packing, fumigation and immersion with the chemical used.

Careful control of mycotoxins should be started and administered by the government of each country through ministries and organizations such as the Ministry of Health, the Ministry of Agriculture, Food and Drug Administration, National Environment Committee Board and Consumer Protection Committee Board. The control program may be set up by a special administrative committee and the legislative body who regulate the national policy of food safety and the maximum tolerance limits for mycotoxins. Farmers, middlemen, food and feed factories and exporters will be well educated about mycotoxins and encouraged to prevent and control the contamination of microflora and their health-hazardous mycotoxins in their commodities as much as possible.

International cooperation for the mycotoxin regulation in trading products or commodities is also needed. The countries should establish quality control limits for certain commodities intended for export or import. The producer countries would be stimulated to be aware of mycotoxin contamination in their exported susceptible commodities.

For example, the European Economic Community EEC has already established certain maximum tolerance limits of aflatoxins for animal feeds, i. Guidelines for international trade include: a procedure of sampling and analysis, b surveillance and food control inspection systems, c use of contaminated produce in feeding of different animals, d protocols for detoxification and the quality control of the products.

Conferences, symposiums, trainings and workshops on current informations of mycotoxins should be promoted. Low-cost technology for assessment, prevention and control of environmental mycotoxins could be then transferred from developed countries to developing ones. Several effective ways for prevention and control hazardous fungi and their dangerous mycotoxins have been presented.

The methods include biological control and physical and chemical treatments. Emmy Koeleman 26 Feb Emmy Koeleman 18 Aug Ines Taschl 15 Feb Emmy Koeleman 29 May Rui Goncalves MSc 17 Jan Emmy Koeleman 22 Oct Emmy Koeleman 12 Oct The contamination of feeds and raw materials by mycotoxins is increasing on a global basis. While the effect of mycotoxins is well known in most terrestrial farm animals the effect of mycotoxins on aquaculture species has not been studied extensively.

Nevertheless, several studies reported pathological signs of mycotoxin poisoning in fish and shrimp species which can cause economic losses to the industry.

Screening for Mycotoxins in Food and Animal Feed

He currently works as aquaculture specialist at Biomin. Most of the mycotoxins that have the potential to reduce growth and health status of fish and other farmed animals consuming contaminated feed are produced by Aspergillus, Penicillium and Fusarium sp. The major classes of mycotoxins include the aflatoxins, trichothecenes, fumonisins, zearalenone and ochratoxins1.

Aflatoxins are produced by Aspergillus fungi, which can infect many potential feedstuffs as corn, peanuts, rice, fish meal, shrimp and meat meals2. Aflatoxin B1 AFB1 is one of the most potent, naturally occurring, cancer-causing agents in animals. Initial findings associated with aflatoxicosis in fish include pale gills, impaired blood clotting, anemia, poor growth rates or lack of weight gain. The extent of disease, caused by consumption of aflatoxins, depends upon the age and species of the fish. Fry are more susceptible to aflatoxicosis than adults and some species of fish are more sensitive to aflatoxins than others3.

The carcinogenic or toxic effects of aflatoxins in fish seem to be species specific. While Rainbow trout are extremely sensitive to AFB1, warm water fish such as channel catfish Ictalurus punctatus are reported to be less sensitive to aflatoxins5. Although less sensitive, warm water species are still affected by aflatoxin contamination. In carp, it was reported that aflatoxins are potential immuno-suppressors7. A recent study 8 indicated that feeding diets containing aflatoxins from moldy corn does not seem to affect channel catfish weight gain, feed consumption, feed efficiency, and survival.

Studies on the Nile tilapia Oreochromis niloticus showed reduced growth rates when tilapias were fed diets containing ppb AFB In addition, tissue abnormality or lesions in the livers of these tilapias showed the beginnings of cancer development. In another study, Nile tilapia fed diets with 0. A more recent study11 showed that acute and sub-chronic effects of AFB1 to Nile tilapia are unlikely if dietary concentrations are 0. However, diets containing levels of AFB1 higher than 0. Diets containing ppm AFB1 caused weight loss and severe hepatic necrosis in Nile tilapia Other studies have shown that tolerance levels for tilapia can vary with the production system.

In green water and flow-through systems, the presence of aflatoxins at 25 to 30 ppb in the water decreased growth without any noticeable signs of mortality. However, in cage culture, concentrations of aflatoxins above 5 ppb caused an increase in mortality rates In marine shrimp, several studies showed that AFB1 can cause abnormalities such as poor growth, low apparent digestibility, physiological disorders and histological changes, principally in the hepatopancreatic tissue14,15,16, Nevertheless, reports on the effect of AFB1 on shrimp are inconsistent.

A study in reported that after just 7 or 10 days of consumption of diets with AFB1 levels below 20 ppb, mortality rate was slightly higher in AFB1-treated groups than in the control group. Histopathological findings indicated hepatopancreatic damage by AFB1 with biochemical changes of the haemolymph. In another study, AFB1 at 50— ppb showed no effect on growth in juvenile shrimps However, growth was reduced when AFB1 concentrations were elevated to — ppb.

Survival dropped to There were marked histological changes in the hepatopancreas of shrimp fed diet containing AFB1 at a concentration of — ppb for 8 weeks, as noted by atrophic changes, followed by necrosis of the tubular epithelial cells. Severe degeneration of hepatopancreatic tubules was common in shrimp fed high concentrations of AFB According to a study in , the effect of AFB1 toxicity to shrimp results in the modification of digestive processes and abnormal development of the hepatopancreas due to exposure to mycotoxins.

Ochratoxins are a group of secondary metabolites produced by fungal organisms belonging to Aspergillus and Penicillium genera. Ochratoxin A OA is the most abundant of this group and is more toxic than other ochratoxins. Very few studies have been conducted to determine the effect of ochratoxins in fish species. In juvenile channel catfish, diets containing levels of 1 to 8 ppm of OA resulted in the development of toxic responses. Significant reduction in body weight gain were observed after only 2 weeks in fish fed diets containing 2 ppm of ochratoxin A or above After 8 weeks body weight gain was significantly reduced for fish fed diets containing 1 ppm OA or above.

Additional toxic responses included poorer FCR for fish fed diets with 4 or 8 ppm OA, and lower survival and hematocrit count for fish fed the 8 ppm OA diet. Severe histopathological lesions of liver and posterior kidney were observed after 8 weeks for catfish fed diets containing levels of OA of 4 and 8 ppm