**1. Introduction**

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128 Aflatoxins - Recent Advances and Future Prospects

*2004/007243*.

Mycotoxins are the toxic products of fungal metabolism occuring in a wide variety of com‐ modities like animal feeds and human food products. Mycotoxins on ingestion can cause health hazards both in livestock and human beings and hence there is a greater economic and public health implication. The severity of mycotoxin contamination is determined by environmental factors like excessive moisture in the field as well as in storage, hot and hu‐ mid climate and insect infestation. Mycotoxin contamination of feed affects practically all livestock but greater information is available on dairy cattle, poultry, and swine. In these an‐ imals mycotoxins reduce production efficiency, impairs resistance to infection and compro‐ mise reproduction. Economic losses due to mycotoxicosis are derived directly from livestock morbidity, mortality and wastage of contaminated feed. On a global scale, it is estimated that around 25% of the world's crops are affected by mycotoxins annually and in addition to the above losses costs involved in monitoring the level of mycotoxins should also be consid‐ ered. The recent mycotoxin surveys have indicated that the percent contamination is much higher than the perceived 25%. The mycotoxins that are of significance in animal feed are: Aflatoxins, Ochratoxins and Fusarial toxins (Fumonisins, Zearalenone, Trichothecenes in‐ cluding Deoxynivalenol and T-2 toxin).

## **1.1. Aflatoxins and biological action**

The aflatoxins are highly toxic and carcinogenic compounds produced by *Aspergillus* fungi at an optimum temperature of 25-320 C, moisture of greater than 12-16% and a relative hu‐ midity of 85%. Commonly affected feeds are maize, groundnut cake, cottonseed cake and copra cake and causes toxicity in poultry, cattle, sheep and swine. Animal consuming afla‐ toxin contaminated feed display poor performance, reduced immunity, liver damage, kid‐

ney and intestinal haemorrhage and liver tumors. Among the afltoxins B1 is more prevalent and toxigenic. This is metabolized to Aflatoxin M1 in liver and is excreted in milk of dairy cattle and also as residue in egg / meat.

**2. Control and counteraction of aflatoxins**

Aflatoxins affect mainly liver and kidney and are also carcinogenic and mutagenic (Fig 1). Therefore effective control and detoxification measures need to be undertaken. Toxin pro‐ ducing fungi may invade at pre-harvesting period, harvest-time, during post harvest han‐ dling and in storage. According to the site and time of infestation, the fungi can be divided into three groups: (a) Field fungi (b) Storage fungi (c) Advanced deterioration fungi. Field fungi are generally plant pathogenic fungi; namely *Fusarium*. The storage fungi are *Aspergil‐ lus* and *Penicillium*. The advanced deterioration fungi, normally do not infest intact grains but easily attack damaged grains and requires high moisture content, that include *Aspergil‐*

Recent Advances for Control, Counteraction and Amelioration of Potential Aflatoxins in Animal Feeds

http://dx.doi.org/10.5772/51779

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Prevention and effective plan for reducing fungal growth and toxin production is very im‐ portant. The recommended practices include 1. Development of fungal resistant varieties of plants, 2. Suitable pre-harvest, harvest and post harvest techniques, 3. Store commodities at low temperature as for as possible, 4. Use fungicides and preservatives against fungal

growth and 5. Control of insect damage in grain storage with approved insecticides.

**2.1. Preventive measures**

*lus clavatus*, *Aspergillus fumigatus*.

**Figure 1.** Mechanism of cell damage in mycotoxin toxicity.

(adopted from Joshua M Baughman and Vamsi K Mootha, 2006) [6]

The secondary prevention of fungal growth include limiting the growth of infested fungi by re-drying the product, removal of contaminated seeds. The tertiary measures could be to prevent the transfer of fungi and their health hazardous toxins into the food/feed and to the

Epoxide derivative of aflatoxin B1 binds with DNA and disrupts transcription and transla‐ tion activities, thus initiating carcinogenesis. Oxidative nature of the toxic derivative releas‐ es free radicals and cause cell damage (Fig.1). Advancement in molecular techniques like microarray and PCR has helped to understand the precise mechanism of action of aflatoxin. Recent gene expression studies have shown that down regulation of mitochondrial carnitine palmitoyltransferase (CPT) system, down regulation of fatty acid metabolism pathway, upregulation of cell proliferation pathway and down regulation of B cell activation are respec‐ tively responsible for decreased body weight gain, fatty liver / increased liver weight, carcinoma and lowered immunity in birds fed aflatoxin. Supplementation of curcumin through turmeric powder ameliorated most of the ill effects induced by aflatoxin. Adverse effects of aflatoxicosis are much severe when there is a concurrent contamination with other toxins like ochratoxin and T-2 toxin.

#### **1.2. Limits of aflatoxin**

The presence of Aflatoxin M1 in food products meant for human consumption is not desira‐ ble and the residual concentration should not exceed 0.5 ppb as per FDA regulations. Such regulations are much more stringent in European Union where the level should not exceed 0.05ppb. Aflatoxin B1 level of 20 ppb in the diet of dairy cattle is appropriate for reducing the risk of aflatoxin M1 in milk. In many countries there are strict guidelines for maximum toler‐ able limits of aflatoxins, beyond which the commodity is unsafe and not accepted (Table 1).


**Table 1.** Suggested limits for aflatoxin.
