A PRACTICAL STABLE RATIONAL BIOSOLUTION
TO DESTROY TOXINS
• Enhances nutrient digestion and absorption
• Halts growth of pathogenic microbes and moulds
• Improves feed intake
• Reduces damages to Liver and G I Tract membrane
• Simulates Immune System
• Starts functioning when once comes into contact with the feeding stuff
• And continues to perform in the G I tract and at the Hepatic Level.
Fungi (Myces) are plant-similar micro organisms, some of them are large sized (as mushrooms) and the others are microscopic, therefore they are poly-or-mono-cellular. Some of the fungi are useful for man, since they could be eaten or used in producing drugs, dairy products, bread…. etc., and used in fungal biocontrol. Yet, the others are harmful for man, animals and plants, since they cause diseases (mycoses) and / or intoxications (mycotoxicoses). Therefore, fungi are responsible for crops damage (25% of the yearly production), whether in the field, during transportation, and / or during storage. Toxic fungi can also invade various feed - and foodstuffs and hence affect agricultural animals (Abdelhamid and Saleh, 1996) and humans (Abdelhamid et al., 1999). Moreover, these toxigenic fungi occur also in and / or on moist houses, libraries, air conditioners, feed mills, dust, air, insects, temples, banknotes, and computer disks and compact disks (Abdelhamid, 1998, 1999-b, and 2000-b).
It is a fungal toxin, i.e. it is a secondary toxic - metabolite which produced from a toxigenic fungus. Any mycotoxin could be produced from many fungal species, and any fungal strain can produce many mycotoxins. Therefore, any moldy sample may contain numerous fungal genera and species (multi-infection), hence and consequently it may be contaminated with different mycotoxins.
For instance, zearalenone (F-2) is produced by Fusarium roseum, F. tricinctum, F. oxysporum, and F. moniliforme. Also, diacetoxyscirpenol (DAS) producing fungi are F. equiseti, F. sambucinum, F. tricinctum, F. scirpi, F. solani, F. rigidiusculum, F. culmorum and F. avenaceum. On the other hand, A. ochracious produces aflatoxins, ochratoxins, penicillic acid, cycalonic acid, viomllin….. etc., and A. flavus produces, aflatrime, aflatoxins, aspergillic acid, aspertoxin, cyclopiazonic acid, kojic acid, penetrimes, rubratoxins, sterigmatocystin, tremorgns etc. So, when one mycotoxin is detected, man should suspect that others are also present in a contaminated feed (Abdelhamid, 2000-b). However, the story of mycotoxins is very new comparing with the old known story of fungi. It began with the detection of ergot, trichothecines, aflatoxins…. and recently fumonisins. Nowadays, more than one thousand different chemically identified mycotoxins are isolated. They are of low molecular weights. Some of them acts with each other synergistically as fumonisin-B1 and aflatoxin-B1, ochratoxin-A and aflatoxin, T2 toxin and aflatoxin. Mycotoxins cause a wide variety of adverse clinical signs depending on the nature and concentration of mycotoxins present, duration ofexposure, the animal species, its age and nutritional and health status at the time of exposure to contaminated feed (Horvath, 1998).
They are peptide derivatives (Cyclochoritme, Ergot, Gliotoxin, Sporidismine), quinone derivatives (Lotuskirin, Rogulosin), peron derivatives (Aflatoxin, Citrinin, Kojic acid, Sterigmatocystin), terpine derivatives (Fusarinone, Satratoxin, Trichothecines, Vomitoxin), nonadrid (Rubratoxin), alkaloid (Lesergic acid, Slaframin), xanthine (Sterigmatocystin), lacton (Patulin, Penicillic acid, Rubratoxin, Zearalenone), botnolid (Patulin), phynol (Zearalenone), glucose (Kojic acid), qumarin (Aflatoxin, Ochratoxin, Sterigmatocystin) as citd by Abdelhamid (2000-b).
WHAT ARE THE IMPORTANT TOXINS AND WHAT ARE THEIR EFFECTS?
Aflatoxin B1 from A. flavous
Increases Embryonic Mortality. Decreases feed efficiency.
Decreases hatchability. Poor Growth.
Reduced RBC. Anemia.
Impaired Blood Clotting. Damage to Liver
Causes Liver Tumors Decreased Immune responsiveness
Increased Mortality Causes Necrosis, basophilia of hepatocytes
Enlarges blood sinusoids in the kidney Necrosis of gastric glands
Causes liver cancer, hepatoma. Reduces Survival Rate
Elevates internal organs indices Causes chromosomal aberrations
Lowers mitotic index of gill cells. Reduces muscles area
Causes accumulation of iron in intestinal mucosa epithelium
cellulartoxic – free-radical and active oxygen producing
Damages the tissues of gills, intestine, liver, subcutaneous tissue and muscle, spleen, kidneys, and brain.
Aflatoxin G1 and G2
Affects circulatory system regurgitation of stomach contents
Aspergillic acid
neurotoxic
Citrinin from P.Citrinum
Carcinogenic nephrotoxic
Damages Kidney and liver heapatotoxic
Citriovuridine
Affects circulatory system
Cyclopiazonic acid
Affects circulatory system necrosis of gastric glands
Neuro toxin. Suppresses Growth
causes accumulations of proteinaceous granules in renal tubular epithelium
Cyclosorine
Affects circulatory system
Deoxynivalenol
Decreases production Induces Liver toxicity
Leads to Death Carcinogenic
Destruxin-A
chromatide plaster
Ferrocarin E
carcinogenic
Fumonisins
Causes Imbalances in reproduction system Results in poorer egg shell quality
Neurotoxic Hepatotoxic
Nephrotoxic Depresses Growth
Lowered Hematocrit increased liver glycogen
increased vacuolation in nerve fibers Reduces red and white blood cell counts Perivascular lymphohistiocytic investment in the brain
Gliotoxin
Immunotoxic Respirotoxic
Lotuskerine
Affects digestive system
Ochratoxin A from A. ochracius
Decreases body weight Causes deformities of the head, tail and eyes.
Reduces feed Intake Necrosis of Liver, Kidney
inhibition of DNA, RNA and protein synthesis Nephrotoxic
Increased incidence and severity of melanomacrophage centers in hepatopancreatic tissue and posterior kidney
Reduction of number of Exocrine pancreatic cells
Oosporein
Nephrotoxic
Rubratoxin
Affects digestive system
Sterigmatocystine
Carcinogenic hepatotoxic
digestive system toxins Reduces Survival Rate
decreases growth rate as well as muscular protein content
T-2 Toxin
Leads to oral lesions, Gizzard lesions Decreases chick weight
Causes dermatitis Decreases Hatchability
estrogenic, sexual disorders Affects circulatory system
Damages the intestinal tracts Causes severe oedema
Causes fluid accumulation in the body cavity and behind the eyes.
loss of the intestinal mucosa Reduced Growth Rate
poor F C R
Trichothecines
Carcinogenic dermal toxic
Vomitoxin
Immunotoxic Neurotoxic
Zeralenone
Lessens feed intake Decreases Growth rate
Results in Fatty Liver Genotoxic
OCCURRENCE OF FUNGI IN FEEDS
A Survey for microorganisms associated with the aquatic and terrestrial animals revealed that more than 20 fungal isolates belonging to different genera and species including Saprolegnia, Trichoderma, Alternaria spp., Penicillium, Fusarium sp., Fusarium semitectum (= F. incarnatum), Cladosporium, Phoma, Nigrospora, Aspergillus niger and Aspergillus flavus were isolated from naturally diseased animals
OCCURRENCE OF MYCOTOXINS IN FEEDS
The most widely found in nature and grow and produce toxins under the proper conditions are fungal genera Aspergillus, Penicillium and Fusarium. The latest genus requires high moisture content, so outspreads in fields and attacks vegetative substances and known as “field fungi”. Whereas, both former genera require low humidity, so are outspreading in store houses and known as “storage fungi”. However, moisture content greater than 14% and relative humidity greater than 70% are required for fungal growth and toxin production. Fungal invasion negatively affects physical (texture, color, odor, flavor) and chemical (mineralization) properties as well as feeding value of the infected feed (Abdelhamid, 1993b; 1995b&c; 1999a; 2000a and 2001 and Abdelhamid et al., 1985).
So, it is economically important to avoid buying damaged (mechanically or moldy) feed stuffs, maintain good conditions in store houses and do not store finished feeds for long periods (Abdelhamid, 1985; 1989 & 1990 and Noonpugdee et al., 1986).
Toxigenic fungi and their toxins are found often in various feeds of plant and animal origins including Aspergillus flavus, A. niger, Mucor, and Pencillium .
The following Table illustrates some feeding stuff and their mycotoxins content (Abdelhamid, 1980, 1983a - e, 1985, 1990, 2000b & 2005 and Abdelhamid et al., 1996):
Feeds Mycotoxins
Bone meal Vomitoxin and Zearalenone
Cottonseed , Rice bran Aflatoxin-B1, Citrinin, Ochratoxin-A, Vomitoxin, and Zearalenone
Grains Aflatoxin-B1 & G1, Citrinin and Ochratoxin-A
Maize Aflatoxin-B1, Fumonisins, Ochratoxin-A and Vomitoxin
Maize flour, beans Aflatoxins, Cyclopiazonic acid, Patulin and Griseofulvin
Maize, pea/Groundnut meal, Aflatoxins, Cyclopiazonic acid, Ochratoxin-A, and Zearlenone
sunflower meal, sorghum, wheat Aflatoxins, Cyclopiazonic acid, Ochratoxin-A and Zearlenone
Maize, Peanut oil Aflatoxin-B1
Milk products Aflatoxins-B1, B2. M1 and Patulin
Rice bran Aflatoxin-B1, Ochratoxin-A, Citrinin, Vomitoxin, Cyclopiazonic acid and Moniliformine
A. flavus producing for aflatoxins was found in dried Jawla, Prawn Head and Shell . Also, A. ochracious, A. flavus, A. tamari and A. niger were found in smoked fish, so smoked fish contain aflatoxins and ochratoxin-A.
Fish meal contained aflatoxin-B1 and ochratoxin-A; hence, sea foods were contaminated with aflatoxin-B1 residues, therefore caused human mycotoxic food poisoning. However, feedstuff samples were tested for the presence of some mycotoxins and found to be contaminated, particularly with vomitoxin, aflatoxin, citrinin, zearalenone and ochratoxin, in descending order concerning the percentage of rejected (highly contaminated than the tolerable level) samples. Feeds were heavily contaminated with aflatoxin up to 3388 ppb (Abdlhamid et al., 1997). However, co-occurrence of cyclopiazonic acid was found in the aflatoxin-contaminating feed samples (Balachandran and Parthasarathy, 1996). Generally, mold toxins are more toxic to the juveniles of any species (Lim and Webster, 2001).
FACTORS AFFECTING MYCOTOXINS PRODUCTION
Each fungus requires special conditions (substrate, moisture, temperature….) for its growth and other conditions for its toxin(s) production which are different than those of the other fungi and toxins. However, the main affecting factors on toxin production are genetic factors (related to the fungus, its strain and its genetic capability) and environmental factors including:
1. The substrate (on which the fungus will grow) and its nutritious content.
2. Water content {water activity (aw)} of the substrate and ambient relative humidity.
3. Ambient temperature (dry growing season).
4. Ambient oxygen content (is required for fungal growth).
5. Ambient carbon dioxide (not required for fungal growth).
6. Mechanical damage (enable fungal invasion and mycotoxin production).
7. Insects invasion (enable fungal invasion and mycotoxin production).
8. Increased count of fungal spores accumulates the produced mycotoxin.
9. The growth of non-toxic fungal strains inhibits the production from the toxigenic fungi.
10. Presence of specific biota inhibit growth of fungi and mycotoxin production.
11. Time of fungal growth (after the plateau , the capability of producing toxins decreases).
12. Cultivation operations [plants density/area unit (micro clime), agricultural rotation,
13. fertilization, wet harvest, mechanization, storage period….. etc.].
14. Low layer thickness of a crop (< 50 cm) during drying strongly decreases mycotoxin production (Abdelhamid, 2000-b).
MYCOTOXINS DETECTION
The method of mycotoxin analysis depends mainly on the mycotoxin it self (or its metabolites) and the contaminated tissue or substance will be tested. Therefore, there are many detection methods for each mycotoxin, and there are screening methods for detecting more than one mycotoxin simultaneously in the same sample. However, each method has specific accuracy, sensitivity, recovery and reproducibility within a specific range of the mycotoxin levels (Abdelhamid, 1981, 1995a and 1996).
The principles of analysis consist of precise sampling, sample preparation and toxin extraction, purification, derivation, elution, concentration, qualitative detection, confirmation, and quantitative detection.
Methods of mycotoxins examination include
biological methods (e.g. cells, tissues, eggs, shrimp, fish, chicks…etc),
physical methods (e.g. UV-light),
physico-chemical methods {e.g. spectrophotometer and chromatography (Paper, Column, TLC, HPTLC, LC, HPLC, GLC – MS)}
and immuno-enzyme methods, e.g. ELISA
(Schweighardt et al., 1980-a & b and Abdelhamid, 1985, 1996 & 2000-b).
FACTORS AFFECTING SEVERITY OF A MYCOTOXIN
It may be affected by many factors including the mycotoxin it self, level of contamination (chronic, sub acute, acute), time of exposure, route of application, presence of other mycotoxins, the organism exposes to a mycotoxin (genetic effect on the enzyme system), sex and age of the exposed organism (hormonal effect), and clinical status of the exposed organism (hepatic enzymes status) (Abdelhamid, 2000-b).
Toxin LD50
Aflatoxin-B1 0.5
Aflatoxin-B1 0.5 (mg/Kg body weight)
Aflatoxin-B1 0.08 (mg/Kg body weight)
Aspertoxin 6.6
Grusiofolvin 0.28
Ochratoxin-A 1.7
Ochratoxin-A 3.0 (mg/Kg body weight)
Ochratoxin-B 13.0 (mg/Kg body weight)
Patulin 18
Stemfon 1.2
Sterigmatocystin 0.24
Sterigmatocystin 137 (ppb in diet)
T-2 toxin 6.5 (mg/Kg body weight)
PROPHYLAXIS AND TREATING
Prophylaxis is more better, easier, cheaper and realizable than treating (curing) mycotoxin. Therefore, preventing fungal invasion is a must because there are no effective means for overcoming mycotoxins and their negative effects (Lee, et al., 1969; Wellford, et al., 1978; Abdehamid, 1993a; Abdelhamid and Mahmoud, 1996; Horvath, 1998; Abdelhamid et al., 2002a; Heiler and Schatzmayr, 2003 and Shehata et al.,2003a & b). However, it could be beneficial to alleviate these effects through one or more of the following steps:
separation, screening, washing, heating, roasting, microwave,
HOW CAN THE MYCOTOXINS BE DEGRADED?
Aflatoxin AFB1 and Ochratoxin OA can be degraded by Enzymes like REDUCTASE and DEHYDROGENASE.
Tricothecenes T2 are degraded by EPOXIDASE
Zearalenone is degraded by LACTONASE
WHAT TOXIBINDBIO CONTAINS?
Acetobacter Xylinum Activated Carbon Alum pulvis Bacillus Subtilis
Benzoic acid black peper Dhaniya Crude Pulvis citric acid
chitin isolated from crustacean shells clove oil Dextrose Eclipta alba
garlic powder Honey Tulsi crude pulvis L acidophilus
Hydrated Sodium alluminium Silicate Nigella sativa plumbago indica S. boulardi
Sodium bicarbonate Sodium Hydroxide Spirulina T.Viride
Mannon Oligo Sacharides, 1,3/ 1,6 beta glucans Swertia chirraita Thio Urea Thymol,
cinnamon containing trans-cinnamic acid, trans-cinnamaldehyde, and ferulic acid (phydroxy-3-methyl cinnamic acid)
WHAT IS THE MODE OF ACTION OF TOXIBIND BIO?
Physical means of adsorption of the toxins is achieved by the Activated Carbon and Hydrated Sodium Aluminum Silicate.
Chemical means of honey, garlic, ammonia, Sodium Hydroxide, Sodium Perborate, Calcium Peroxide; Potassium Bi sulfate and sugars (for reduction), propionic Acid, Benzoic Acid are also employed to act on contact.
Biological means (biotransformation) (by fungi, yeasts and bacteria) are also employed to work at the gut level and hepatic level..
Trichoderma viride is a promising biocontrol agent for the pathogens, Saprolegnia sp. and Aspergillus ochraceus. It can significantly reduce saprolegniasis severity. It is safe and is also used for biological control purposes against pathogens. S boulardi by secreting H2O2 will oxidize and destroys the toxins.
Dietary means like vitamins (A, E) and minerals (Se) help in fighting the toxins and bring down the severity of the problem.
Addition of Thiourea and Organic Acids capable of destroying the fungi and impairing their ability to produce toxins; in TOXINBIND BIO is made with the sole purpose of providing a synergetic effect and to provide consistent results.
Medicinal Herbs like Cinnamon, Tulsi, Thymol, Menthol are well known Fungicides and they are well documented to combat toxicosis.
Pepaver acts on the CNS of the flukes and makes them to loose their grip and fall into water medium unconscious.
Coriander Seed, Methi inhibit the fungal metabolism.
Activated Carbon can effectively alleviate lesions of AFB1 (Mohamed and Mokhbatly, 1997.
Nigella sativa significantly ameliorated the adverse effects of dietary AFB1
(Hussein et al. (2000) )
ALUMINUM SULPHATE significantly reduces the amount of AFB1 absorbed from the digestive system following ingestion. ( Ellies et al. (2000) )
Feeding of 1,3/1,6 Beta glucan significantly raised the degree of resistsnce against A. hydrophila challenge and the non-specific immunity level. (Sahoo and Mukherjee, 2001a)
Mannon Oligo Sacharides binds the mycotoxins.
Effects of Clay, Auto claved egg shells, Auto Claved shrimp shells and betaine are significant in overcoming the aflatoxic symptoms (on growth, mortality, feed utilization, organs indices, carcass composition and blood enzymes).
Anti Oxidants present in TOXIBIND BIO minimizes the resynthesis of mycotoxins at the Hepatic level.
TOXIBIND BIO contains Mould inhibitors too.
Enzymes produced by the Beneficial Microbes in TOXIBIND BIO degrade the toxins.
Thus stopping of secretion of toxins by pathogens, destroying of the pathogens, degrading the toxins, removal of mycotoxins from the contaminated feeding stuff besides the resulting changes in physical and nutritional properties of these feeding stuffs are well taken care in TOXIBIND BIO.
HOW DOES TOXBIND BIO IS SUPERIOR WHEN COMPARED TO OTHER TOXIN BINDERS AVAILABLE IN THE MARKET?
• Withstands Pelletisation Temperatures
• Dominates And Controls All Pathogens Like Aspergillus, Fusarium,
• Claviceps Spp., P. Citrinum, P. Viridicatum, Salmonella, E Coli, Pasteurella.
• Produces Several Useful Enzymes To Improve F C R
• Transforms the Mycotoxins In The Desired Pathway.
• Destroys and Degrades The Toxins In A Unique Efficient Manner.
• Controls Pesticide and Other Chemical Toxicity.
• Acidifies Gut
• Consumes The Toxins And Converts The Same Into TDN
• Improves Daily Body Weight Gain
• Reduces Mortality Rate
• Detoxifies Faster In A Complete And Efficient Way
DOSAGE:
Preventive: 250 gms/ Ton Feed for every 0.5% Moisture in excess of 7% Moisture in the end product.
Curative: 500 gms/ Ton Feed for every 0.5% Moisture in excess of 7% Moisture in the end product for five days.
REFERENCES:
Abdelhamid, A.M., Afaf. M. Fayed, A.Z. Ghanem and H.G. Helal
Abdelhamid, A.M. (1983-a). Existence of zearalenone (F2) in the Egyptian foods and feeds. In: Proceedings of the 1st African Conference of Food and Technology, Cairo, pp: 592 – 603.
Abdelhamid, A. M. (1983-d). Occurrence of vomitoxin in some Egyptian foods and feeds. In: Abstracts book of the International Mycotoxin Conference, Cairo, No. 59.
Abdelhamid, A.M.; A.I. Mehrim and F.F. Khalil (2003). Detoxification of aflatoxin – contaminated diet of tilapia fish using dietary supplementation with egg shell, Betafin, clay or silica. Proc. 1st Egypt. – Syrian Conf., El-Menia Univ., Egypt, 8 – 11 Dec.
Abdelhamid, A.M.; A.M. El-Mansoury, A.I. Osman and S.M. El-Azab (1999). Mycotoxins as causative for human food poisoning under Egyptian conditions. J. Agric. Sci., Mansoura Univ., 24: 2751 – 2757.
Abdelhamid, A.M.; E.A. Sadik and E.A. Fayzalla (1985). Preserving power of some additives against fungal invasion and mycotoxin production in stored-crushed-corn containing different levels of moisture. Acta Phytopathologica Academca Scientiarum Hungaricae, 20: 309 – 320.
Abdelhamid, A.M.; F.F. Khalil and M.A. Ragab (1996). Survey of aflatoxin and ochratoxin occurrence in some local feeds and foods. Proceeding of conference on Foodborne Contamination and Egyptian’s Health Conference, Mansoura Univ., Egypt, Nov. 26
Abdel-Wahhab, M.A.; A.M. Hasan, S.E. Aly and K.F. Mahrous (2005). Adsorption of sterigmatocystin by montmorillonite and inhibition of its genotoxicity in the Nile tilapia fish (Oreochromis niloticus). Genetic Toxicology and Environmental Mutagenesis Armbrecht, B.H. (1972). Aflatoxin residues in food and feed derived from plant and animal source. Residue Rev., 41: 13 – 54.
Balachandran,C. and K.R. Parthasarathy (1996). Occurrence of cyclopiazpnic acid in feeds and feedstuffs in Tamil Nadu, India. Mycopathologia,
Chavez-Sanchez, M.C., C.A. Martinez-Palacios, I. Osorio – Mareno, C.A.M. Palacios and I.O. Moreno (1994). Pathological effects of feeding young Oreochromis niloticus diets supplemented with different levels of aflatoxin B1. Aquaculture, 127: 49 – 60.
Coma, J. (2002). Securing feed from salmonella. Feed Tech, 6 (2) : 16 – 19 . Dollar,
Eisa, N. A., S. K. Abdel – Reheem, G. M. El – Habbaa, F. M. Emara and M. F. Abou – El – Ella (2002). Studies on maize grains deterioration under Egyptian conditions – corn kernel damage percentage and application of some control techniques. Proc. 2nd Conf. Foodborne Contamination & Egyptian's Health, 23 – 24 April, pp: 53 – 65.
Essa, M.A.A., K.M. Soliman and H.M.F. El-Miniawi (1998). Fix –A – Tox in aquaculture. II. Monitoring the preventive effect of Fix – A – Tox against aflatoxicosis in cultured Oreochromis niloticus. Vet. Med. J., Giza, 46 (3) : 267 – 284.
Goldblatt, L. A. (1976). Significance of aflatoxin in foods. Proc. 80th Annual Conference of the Association of Food and Drug Officials, Atlanta, Georgia, June 22, pp: 191 – 201.
Halver, J.E. (1969). Aflatoxicosis and trout hepatoma. In: L.A. Goldblatt (ed.) Aflatoxins. New York, Academic Press.
Heidler, D. and G. Schatzmayr (2003). A new approach to managing mycotoxins. World Poultry, 19 (2) : 12 – 15.
Horvath, E.M. (1998). Taking the threat out of mycotoxins. Feed Tech, 2 (1) : 32 – 33.
Hussein, S.Y.; I.A.A. Mekkawy, Z.Z. Moktar and M. Mubarak (2000). Protective effect of Nigella sativa seed against aflatoxicosis in Oreochromis niloticus. Proc. Conf. Mycotoxins and Dioxins and the Environment, Bydgoszcz, 25 – 27 Sept., pp: 109 – 130.
Jantrarotai, W., and R.T. Lovell (1990b). Acute and subchronic toxicity of cyclopiazonic acid to channel catfish. J. Aquatic Animal Health, 2 (4) :
Lee, L.S.; A.F. Cucullu, A.O. Fraz, Jr., and W.A. Pons, Jr. (1969). Destruction of aflatoxins in peanuts during dry and oil roasting. J.Agr. Food Chem., 17 (3) : 451 – 453.
Li, M.H., S.A. Raverty and E.H. Robinson (1994). Effects of dietary mycotoxins produced by the mold Fusarium moniliform on channel catfish Ictalurus punctatus. J. World Aquaculture Soc., 25 (4) : 512 – 516.
Lim, H., W. Ng, S. Lim and C.O. Ibrahim (2001). Contamination f palm kernel meal with Aspergillus flavus affects its nutritive value in pelleted feed for tilapia, Oreochromis mossambicus. Aquaculture Research, 32 (11) : 895 – 905.
Lumlertdacha , S. and R.T. Lovell (1995). Fumonisin-contaminated dietary corn reduced survival and antibody production by channel catfish challenged with Edwardsiella ictaluri. Journal of Aquatic Animal Health, 7 : 1 – 8.
Mahmoud, K.I.; A.M. Abdelhamid and A. Mandour (1994). In vitro and in vivo comparative studies on the efficacy of some aflatoxin-detoxifying agents. Alex. J. Vet. Science, 10: 39 – 47.
Marasas, W.F.O.; J.R.Bamburg, E.B.Smalley, F.M.Strong, W.L.Ragland, and B.E.Degurse (1969) . Toxic effets on trout , rats and mice of T-2 toxin produced by the fungus Fusarium tricinctum (Bd.) Snyder et Hansen.Toxicol. and Appl. Pharmacol.,15 : Mohamed, M.H. and A.A. Mokhbatly (1997). Pathologic and immunologic evaluation of activated charcoal in treatment of experimental aflatoxicosis-B1 in Tilapia nilotica. Egypt. J. Comp. Path. Clin. Path., 10 (2) : 169 – 185.
Palti, J. (1978). Toxigenic Fusaria, their Distribution and Significance as Cause of Disease in Animal and Man. Verlag Paul Parey. Berlin und Hamburg.
Prasad, B.N.; B.K. Sinha and A.K. Sinha (1987). Aflatoxigenic fungi isolated from fish and its public health importance. Indian J. Comp. Microbiol. Immunol. Infect. Dis., 8(3) 135 – 136.
Sahoo, P.K. and S.C. Mukherjee (2001a). Effect of dietary beta-1,3 glucan on immune responses and disease resistance of healthy and aflatoxin B1 –induced immunocompromised rohu (Labeo rohita Hamilton). Fish & Shellfish Immun., 11 (8) : 683 – 695.
Sahoo, P.K. and S.C. Mukherjee (2001b). Immunosuppressive effects of aflatoxin B1 in Indian major carp (Labeo rohita). Comparative Immun., Microbi.,Infectious Diseases, 24 (3) : 143 – 149.
Sahoo, P.K. ; S.C. Mukherjee, S. Mohanty, S. Dey and S.K. Nayak (1999)). A preliminary study on acute citrinin toxicity in rohu (Labeo rohita) fingerlings. Indian J. Comp. Microbi., Immun., Infectious Diseases, 20 (1) : 62– 64.
Scarpelli, D.C. (1967). Ultrastructural and biochemical observations on trout hepatoma. Trout Research Conf., Research Rept.,
SCF (2000). Opinion of the scientific committee on food on fusarium toxins. Part 3 : fumomisin B1 (FB1) . European Comission, SCF / CS / CNTM / MYC / 24 Final, Brussel – Belgium.
Schweighardt, H.; J. Böhm, A.M. Abdelhamid und J. Leibetseder (1980-a). Analysis of the fusariotoxins zearalenone and vomitoxin (deoxynivalenol) in human foods and animal feeds by high performance liquid chromatography (HPLC). Chromatographia. 13: 447 – 450.
Shehata, S. A .; A. A. Askar and M. S. Mohamed (2003a). Reduction of the dietary toxicity of T-2 toxin and diacetoxyscirpenol (DAS) by garlic in fish. J.Agric. Sci. Mansoura Univ., 28 : 7169 – 7182.
Shehata, S.A.; M.S. Mohamed and G.. Mohamed (2003b). Reducing the toxicity of aflatoxin B1 by differing adsorbents in fish. J.Agric. Sci. Mansoura Univ., 28 : 7157 – 7167.
Smalley, E.B. (1973). T-2 toxin. J. Amer. Vet. Med. Ass., 163 : 1278 – 1281.
Wellford, T.E.T.; T. Eadie and G.C. Llewellyn (1978). Evaluating the inhibitory action of honey on fungal growth, sporulation, and aflatoxin production. Z. Lebensm. Unters. – Forsch., 166 : 280 – 283.
Ziggers , D. (2002) . Wheat . Feed Tech , 5 (1) : 16 – 21.
