1) Aflatoxins are toxic and carcinogenic substances produced by fungi that can contaminate foods like cereals, nuts, and spices.
2) Humans and animals are primarily exposed to aflatoxins through diet, but occupational exposure is also possible.
3) Aflatoxins like AFB1 are potent liver carcinogens that are metabolized and can form DNA adducts, causing mutations that may lead to liver cancer. Exposure to high doses can cause acute toxicity while long term low exposure risks chronic effects like immune suppression.
Mycotoxins are toxic compounds that are naturally produced by certain types of moulds (fungi). Moulds that can produce mycotoxins grow on numerous foodstuffs such as cereals, dried fruits, nuts and spices. ... Mycotoxins appear in the food chain as a result of mould infection of crops both before and after harvest.Mycotoxins are toxic compounds that are naturally produced by certain types of moulds (fungi). Moulds that can produce mycotoxins grow on numerous foodstuffs such as cereals, dried fruits, nuts and spices. ... Mycotoxins appear in the food chain as a result of mould infection of crops both before and after harvest.
mycotoxins are related to toxins produced by fungi.
This slides had all the necessary knowledge and information for mycotoxins which includes aflatoxin and other fungi toxins
Mycotoxins are secondary metabolites of fungi in the plants before or after harvest, which are capable of producing acute or chronic toxic effects (e.g. carcinogenic, mutagenic, and teratogenic) on animals and probably on humans at the levels of exposure.
Several mycotoxins in agricultural products cause health hazards to people and animals and economical problem. Dangerous mycotoxins are naturally present in foods, feeds and our environment. They are pathologically classified as hepatotoxins, nephrotoxins, vomitoxin and neuromuscular toxin, some of which are potentially carcinogenic and mutagenic. Aflatoxin, for example, is the most potent hepatocarcinogen and mutagen among mycotoxins.
Modern mycotoxicology began with the discovery of Aflatoxin in the early 1960s as the chemical compound responsible for causing “Turkey X” disease. Over 100,000 turkeys died in the United Kingdom after ingesting feed containing contaminated peanut meal from Brazil. The disaster concerned also ducklings, calves, and pigs.
Toxic syndromes, resulting from the intake of Mycotoxins by man and animals, are known as mycotoxicosis. Although mycotoxicosis caused by mould Claviceps purpurea have been known for a very long time.
Mycotoxins are toxic compounds that are naturally produced by certain types of moulds (fungi). Moulds that can produce mycotoxins grow on numerous foodstuffs such as cereals, dried fruits, nuts and spices. ... Mycotoxins appear in the food chain as a result of mould infection of crops both before and after harvest.Mycotoxins are toxic compounds that are naturally produced by certain types of moulds (fungi). Moulds that can produce mycotoxins grow on numerous foodstuffs such as cereals, dried fruits, nuts and spices. ... Mycotoxins appear in the food chain as a result of mould infection of crops both before and after harvest.
mycotoxins are related to toxins produced by fungi.
This slides had all the necessary knowledge and information for mycotoxins which includes aflatoxin and other fungi toxins
Mycotoxins are secondary metabolites of fungi in the plants before or after harvest, which are capable of producing acute or chronic toxic effects (e.g. carcinogenic, mutagenic, and teratogenic) on animals and probably on humans at the levels of exposure.
Several mycotoxins in agricultural products cause health hazards to people and animals and economical problem. Dangerous mycotoxins are naturally present in foods, feeds and our environment. They are pathologically classified as hepatotoxins, nephrotoxins, vomitoxin and neuromuscular toxin, some of which are potentially carcinogenic and mutagenic. Aflatoxin, for example, is the most potent hepatocarcinogen and mutagen among mycotoxins.
Modern mycotoxicology began with the discovery of Aflatoxin in the early 1960s as the chemical compound responsible for causing “Turkey X” disease. Over 100,000 turkeys died in the United Kingdom after ingesting feed containing contaminated peanut meal from Brazil. The disaster concerned also ducklings, calves, and pigs.
Toxic syndromes, resulting from the intake of Mycotoxins by man and animals, are known as mycotoxicosis. Although mycotoxicosis caused by mould Claviceps purpurea have been known for a very long time.
Abstract: Aflatoxicosis is among the major cause of economic losses in poultry production. Aflatoxins are a group of hepatotoxic compounds produced by the fungus of Aspergillus sps. when growing on feedstuffs. Aflatoxins are hepatotoxic, mutagenic and carcinogenic fungal toxin which is capable of producing diseases in farm animals as well as poultry. There are four primary aflatoxins: aflatoxin B1 (AFB1), aflatoxin B2 (AFB2), aflatoxin G1 (AFG1) and aflatoxin G2 (AFG2). Among these AFB1 is the most toxic aflatoxin. Aflatoxicosis in poultry is characterized by decreased growth rate, poor feed conversion, immunosuppression, passage of undigested food in the dropping, anemia, decrease egg production in layers quantitatively and qualitatively, decrease hatchability, embryonic mortality, reduced fertility due to decrease testicular weight, decrease semen volume and sometimes there may be lamness, ataxia, convulsions & death. In humans being acute aflatoxicosis is manifested by vomiting, abdominal pain, pulmonary edema, coma, convulsions, and death with cerebral edema and fatty involvement of the liver, kidney and heart. Keywords: Aflatoxin, Poultry, Hepatotoxic.
Title: Aflatoxicosis in Poultry
Author: Sakshi Tiwari, Vikash Sharma, Amrender Nath Tiwari, Amit Shukla
ISSN 2349-7823
International Journal of Recent Research in Life Sciences (IJRRLS)
Paper Publications
Phytotoxin
phtotoxin produce by bacteria and fungi
Bacterial toxin are two types endotoxin and exotoxins
Fungi produce toxin Mycotoxins
Mycotoxins - Aflatoxins B1, B2, G1, G2,
Products contaminated by aflatoxins such as cereal, tree nuts, dry fruits, spices, dairy products, eggs, and medicinal plants.
There are various methods use for the detections of aflatoxins like HPLC, HPTLC, ELISA,TLC, and LC-MS.
Aflatoxins cause chronic and acute toxicity.
Chronic- slow growth, immunity problems, cirrhosis, and liver cancer.
Acute- Hemorrhage, edema and acute liver toxicity.
Does allicin combined with vitamin B-complex have superior potentials than α-...Prof. Hesham N. Mustafa
Background: The current article aims to explore the protective potentials of α-tocopherol
alone and the combination of allicin and vitamin B-complex against lead-acetate
neurotoxicity on the cerebellar cortex.
Materials and methods: Forty rats were divided into four groups (n=10). Group 1 was the
control group. Group 2 received 10 mg/kg body weight (BW) of lead acetate. Group 3 was
exposed to 10 mg/kg BW of lead acetate plus a combination of allicin (100 mg/kg BW)
and vit. B-complex (40 mg/kg BW). Group 4 was administered lead acetate (10 mg/kg
BW) and α-tocopherol (100 mg/kg BW). The animals received treatment for sixty days by
oral gavage. All the groups were studied ultrastructurally and immunohistochemically with
glial fibrillary acidic protein (GFAP).
Results: The affected groups revealed shrunken and degenerated Purkinje cells with
irregular nuclei. The cytoplasm comprised several lysosomes, unhealthy mitochondria, and
dilated Golgi saccules. The myelinated nerve fibers demonstrated breaking of the myelin
sheaths, apparent vacuoles, and broad axonal spaces. Immunohistochemically, there was a
tremendous surge in GFAP-positive astrocytes in the lead acetate-treated group. These
histological and ultrastructural variations were ameliorated by the administration of α-
tocopherol and the combination of allicin and vit. B complex. Moreover, an apparent
decrease in the number of GFAP-positive astrocytes was obvious in the protected groups.
Conclusions: Although both α-tocopherol and the combination of allicin and vit. Bcomplex can be used as possible adjuvant therapies to ameliorate nervous system ailments
attributable to lead acetate, α-tocopherol showed more protective potential.
Key words: Allicin, Purkinje cells, Astrocytes, GFAP, Oligodendrocyte, Myelin Figure
2. Introduction Aflatoxins are one of the most potent toxic substances that occur naturally. These are a group of closely related mycotoxins produced by fungi Aspergillus flavus and A. parasiticus. Aflatoxicosis is poisoning that result from ingestion of aflatoxins in contaminated food or feed. Aflatoxin poisoning is reported from all parts of world in almost all domestic and non domestic animals like cattle, horses, rabbits, and other non human primates. Aflatoxicoses is also reported in humans in many parts of the world. Aflatoxin
3. Exposure to Aflatoxin Diet is the major way through which humans as well as animals are exposed to aflatoxins. Apart from this, exposure to aflatoxin can be through ingestion of contaminated milk containing Aflatoxin M1(metabolite of AFB1). Occupational exposure to aflatoxins in agricultural workers, people working in oil mills, and granaries have been reported.
4. Aflatoxin carcinogenicity After wide experimentation on many animal species like rats, aflatoxin especially aflatoxin B1 is confirmed as a potential carcinogen (IARC 1993). Metabolism plays a major role in deciding the degree of toxicity (Eaton et al 1994). After ingestion, aflatoxin is metabolized by cytochrome p450 group of enzymes in the liver, where it is converted to many metabolic products likeaflatoxicol, aflatoxin Q1, aflatoxin P1, and aflatoxin M1,depending on the genetic predisposition of the species
5. Along with the above another metabolite calledaflatoxin 8,9 epoxideis also formed. Mechanism of action The amount of this metabolite decides the species susceptibility as this can inducemutations byintercalating in to DNA ,by forming an adduct with guanine moiety in the DNA. This intercalation of Epoxide causes a transversion at codon 249 in p53 gene in liver, which may lead tohepatic carcinoma.
9. other nutritional factorsUsing TD50 parameteraflatoxin B1 is 1000 times more potent as a carcinogen when compared to benzo pyrene.IARC has classified Aflatoxin as a group one carcinogen ( IARC 7th annual report on Carcinogens, 1987)
10. Health Aspects Epidemiological, clinical, and experimental studies reveal that exposure to large doses(>6000mg) of aflatoxin may causeacute toxicity with lethal effect whereas exposure to small doses for prolonged periods is carcinogenic. The adverse effects of aflatoxins on animal can be categorized into two general forms. Acute Toxicity Chronic Toxicity
11. Acute Toxicity Acute toxicity is caused when large doses of aflatoxin are ingested. This is common.The principal target organ for aflatoxins is the liver. After the invasion of aflatoxins into the liver, lipids infiltrate hepatocytes and leads to necrosis or liver cell death. This is mainly because aflatoxin metabolites react negatively with different cell proteins, which leads to inhibition of carbohydrate and lipid metabolism and protein synthesis. In correlation with the decrease in liver function, there is a derangement of the blood clotting mechanism, icterus (jaundice), and a decrease in essential serum proteins synthesized by the liver.
12. Other general signs of Aflatoxicosis are edema of the lower extremities, abdominal pain, and vomiting. The most sever case of acute poisoning of aflatoxin was reported in north-west India in 1974 where 25% of the exposed population died after ingestion of the molded maize with aflatoxin levels ranging from 6250 to 15600 mg/kg.
13. Chronic Toxicity This is due to long term exposure of moderate to low aflatoxin concentration. The symptoms include decrease in growth rate, lowered milk or egg production, and immuno suppression. Immuno-suppression is due to the reactivity of aflatoxins with T-cells, decrease in Vitamin K activities, and a decrease in phagocytic activity in macrophages. There is some observedcarcinogenecity, mainly related to aflatoxin B1. Liver damage is apparent due to the yellow color that is characteristic of jaundice, and the gall bladder becomes swollen.
14. PROPERTIES OF AFLATOXIN Natural occurrence:Food products contaminated with aflatoxins include cereal (maize,rice, wheat), oilseeds (groundnut, soybean, sunflower, cotton), spices (chillies, black pepper, coriander, turmeric, zinger), tree nuts (almonds, pistachio, walnuts, coconut) and milk.
15. Physical and chemical properties: Aflatoxins are potent toxic, carcinogenic, mutagenic, immunosuppressive agents, produced as secondary metabolites by the fungus Aspergillus flavus and A. parasiticus on variety of food products. Among 18 different types of aflatoxins identified, major members are aflatoxin B1, B2, G1 and G2. Aflatoxin B1 (AFB1) is normally predominant in amount in cultures as well as in food products.
16. Pure AFB1 is pale-white to yellow crystalline, odorless solid. SOLUBILITY Aflatoxins are soluble in methanol, chloroform, actone, acetonitrile.
17. A. flavustypically producesAFB1and AFB2, A. parasiticusproduceAFG1andAFG2as well asAFB1andAFB2. Four otheraflatoxins M1, M2, B2A, G2Awhich may be produced in minor amounts were subsequently isolated from cultures ofA. flavus and A. parasiticus. A number of closely related compounds namelyaflatoxin GM1, parasiticol and aflatoxicolare also produced byA. flavus. Aflatoxin M1and M2 are major metabolites of aflatoxin B1 and B2 respectively, found in milk of animals that have consumed feed contaminated with aflatoxins.
18. CHEMISTRY Aflatoxins are normally refers to the group ofdifuranocoumarinsand classified in two broad groups according to their chemical structure. difurocoumarocyclopentenone series (AFB1, AFB2, AFB2A, AFM1, AFM2, AFM2A and aflatoxicol) and difurocoumarolactone series (AFG1, AFG2, AFG2A, AFGM1, AFGM2, AFGM2A and AFB3). The aflatoxins display potency of toxicity, carcinogenicity, mutagenicity in the order ofAFB1 > AFG1 > AFB2 > AFG2as illustrated by their LD50 values for day-old ducklings.
19. Structurally thedihydrofuran moiety, containing double bond, and the constituents linked to the coumarin moiety are of importance in producing biological effects. The aflatoxins fluoresce strongly in ultraviolet light (ca. 365 nm); B1 and B2 produce ablue fluorescencewhere as G1 and G2 producegreen fluorescence.
23. Chemical reactions of aflatoxins The reaction of aflatoxins to various physical conditions and reagents have been studied extensively because of the possible application of such reactions to the detoxification of aflatoxins contaminated material.(1) Heat:- Aflatoxins in dry state are very stable to heat up to the melting point. However, in the presence of moisture and at elevated temperatures there is destruction of aflatoxin over a period of time. Such destruction can occur either with aflatoxin in oilseed meals, aflatoxin in roasted peanuts or aflatoxin in aqueous solution atpH 7.Although the reaction products have not been examined in detail it seems likely that such treatment leads to opening of the lactone ring with the possibility of decarboxylation at elevated temperatures.
24. 2) Alkalis: In alkali solutionhydrolysis of the lactone moietyoccurs. This hydrolysis appears to be reversible, since it has been shown that recyclization occurs following acidification of a basic solution containing aflatoxin. At higher temperatures (ca. 100oC) ring opening followed by decarboxylation occurs and reaction may proceed further, leading to the loss of the methoxy group from the aromatic ring. Similar series of reactions also seems to occur with ammonia and various amines.
32. sodium perborate react with aflatoxin and change the aflatoxin molecule in some way as indicated by the loss of fluorescence. The mechanisms of these reactions are uncertain and the reaction products remain unidentified in most cases.
33. (5) Reduction: Hydrogenation of aflatoxin B1 and G1 yields aflatoxin B2 and G2 respectively. Further reduction of aflatoxin B1 by 3 moles of hydrogen yieldstetrahydroxyaflatoxin. Reduction of aflatoxin B1 and B2 with sodium borohydride yielded aflatoxin RB1 and RB2 respectively. These arise as a result of opening of the lactone ring followed by reduction of the acid group and reduction of the keto group in the cyclopentene ring.