Mycotoxins are unavoidable contaminants in foods and feeds and are a major problem all over the world. All mycotoxins are low-molecular-weight natural products produced as secondary metabolites by filamentous fungi.

The major toxins of poultry importance include Aflatoxin, Ochratoxin,Citrinin, oosporin, T2 toxin etc.

Mycotoxicoses underlines simplicity of the source and the complexity of the problem. The fungi producing the chemical residues as mycotoxins are common, simple organisms which have very simple requirements for existence. Nutritional needs are met by a source of carbon and nitrogen; they do require water; all they need oxygen.

Toxins occur most commonly in grains damaged by insects. Usually, high moisture grain, sweating of feed ingredients, defective feed bins, defective waterers or feed spilling in the damp litter promote fungal growth and toxin production. Almost all feed ingredients support fungal growth.

Toxin-producing fungi can infect growing crops as a consequence of insect damage, and may produce toxins prior to harvest, or during harvesting and storage. Groundnut seeds may be invaded by A. flavus before harvest.

Mycotoxins cause a wide range of toxic responses ranging from mortality to subtle effect like immunosuppression and biochemical alterations. However generally for many of most mycotoxins, toxic signs include-

Nutrient draining effect
The mould growth reduces nutrient quality and palatability of feed. Moulds utilize nutrients present in the feedstuff for their metabolism and propagation reducing the nutritional quality as well as the palatability of grain. Energy, crude protein and crude fat contents of mouldy maize may go down up to 5, 7 and 63%, respectively. It also reduces all amino acids, vitamins, viz., A, D, E, K, B , B , B , niacin, pantothenic acid in the diet. T-2 toxin consistently 1 2 6 depressed concentrations of vitamin E in chicken plasma (Coffin and Combs).

Since mycotoxins are natural products, there is a lack in knowledge of metabolic pathways regarding many of the toxins. However, lot of research has been done w.r.t biotranformation and metabolim of few important toxins like aflatoxin B, ochratoxin A, trichothecenes

Absorption: Although quantitative data on absorption are not available at present, aflatoxins being fat-soluble are rapidly absorbed in alimentary tract. When poultry were fed rations containing aflatoxins, residues were detected in the liver, kidney, muscle and adipose tissue. The liver contained the highest concentration.

Mycotoxin Metabolism is divided into two phases. The basic biotrasformation reactions are divided into Phase I consisting of oxidation, reduction and hydrolysis and Phase II in which metabolic end products are conjugated with aminoacids, glucuronic acid or glutathione to facilitate excretion.

Hydroxilation results in derivatives which are generally less toxic and that includes Aflatoxin M1 and Aflatoxin B alpha.Chicken liver 2 produces small quantity of M1 and major portion of B alpha. Aflatoxin 2 B may be converted into aflatoxin 1 M in cattle that may occur in the 1 milk. The concentration of aflatoxin M in the milk of cows is about 300 1 times lower than the concentration of aflatoxin B consumed in the feed.

The formation of the epoxides of aflatoxins is probably the more important form of metabolic activation facilitated by microsomal enzymes of liver. Aflatoxin is activated on the outer nuclear membrane to a form that inhibits RNA polymerase and RNA synthesis. The metabolite is highly reactive, binds covalently to DNA. Mechanistically, it is known that the reactive aflatoxin Aflatoxicol Mycotoxins Metabolism-Phase2 AFLATOXIN-B1 Afla M1 : 10% Afla B2a: 80% Afla8,9-epoxide Conjugated to AAs GSH transferase CY P450 Conjugated to GSH 7 epoxide binds to the N position of guanines.The permeability of mitochondria and lysosomal membranes increases. Many other metabolic functions are inhibited, including protein synthesis, enzyme induction. It has been shown that aflatoxins have immunosuppressive properties, probably related to their inhibitory effect on protein synthesis.

In Phase II metabolism toxin metabolite produced in a phase I reaction are conjugated prior to excretion in the bile or urine. The major conjugating enzymes are known to be microsomal glucuronosyltransferases and cytosolic sulfotransferases, methyltransferases, N-acetyltransferases, glutathione Stransferases and aminoacyltransferases are formed with a toxin or a, metabolites and are detoxified by conjugation with taurocholic and glucuronic acids.

In a nutshell, Cytochrome P450 enzymes convert aflatoxins to the reactive 8,9-epoxide form which is capable of binding to both DNA and proteins. A reactive glutathione S-transferase system found in the cytosol catalyzes the conjugation of activated aflatoxins with reduced glutathione, leading to the excretion of aflatoxin.

As Cytochrome P450 is involved in bioactivation of mycotoxins in deleterious intermediates, that is why working on Phase-2 metabolim i.e to improving glutathione activity makes a scientific sense. Because sensitivity of poultry to mycotoxicity appears to be due to an ''unfortunate combination of very efficient Activation and deficient Detoxification in the liver''.