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Aflatoxins are naturally occurring mycotoxins that are produced by Aspergillus flavus and Aspergillus parasiticus, species of fungi. The name was created around 1960 after the discovery that the source of turkey X disease was Aspergillus flavus toxins. Aflatoxins are toxic and among the most carcinogenic substances known. After entering the body, aflatoxins may be metabolized by the liver to a reactive epoxide intermediate or hydroxylated to become the less harmful aflatoxin M1.
At least 14 different types of aflatoxin are produced in nature. Aflatoxin B1 is considered the most toxic and is produced by both Aspergillus flavus and Aspergillus parasiticus. Aflatoxin G1 and G2 are produced exclusively by A. parasiticus. While the presence of Aspergillus in food products does not always indicate harmful levels of aflatoxin are also present, it does imply a significant risk in consumption. Aflatoxins M1, M2 were originally discovered in the milk of cows that fed on moldy grain. These compounds are products of a conversion process in the animal's liver. However, aflatoxin M1 is present in the fermentation broth of Aspergillus parasiticus.
Aflatoxin-producing members of Aspergillus are common and widespread in nature. They can colonize and contaminate grain before harvest or during storage. Host crops are particularly susceptible to infection by Aspergillus following prolonged exposure to a high-humidity environment, or damage from stressful conditions such as drought, a condition that lowers the barrier to entry.
The native habitat of Aspergillus is in soil, decaying vegetation, hay, and grains undergoing microbiological deterioration, and it invades all types of organic substrates whenever conditions are favorable for its growth. Favorable conditions include high moisture content (at least 7%) and high temperature.
The toxin can also be found in the milk of animals that are fed contaminated feed.
International sources of commercial peanut butter, cooking oils (e.g. olive, peanut and sesame oil), and cosmetics have been identified as contaminated with aflatoxin. In some instances, liquid chromatography-tandem mass spectrometry (LC-MS/MS), and other analytical methods, revealed anywhere from 48–80% of selected product samples as containing detectable quantities of aflatoxin. In many of these contaminated food products, the aflatoxin exceeded U.S. Food and Drug Administration (FDA), or other regulatory agency, safe limits.
High-level aflatoxin exposure produces an acute hepatic necrosis, resulting later in cirrhosis, or carcinoma of the liver. Acute hepatic failure is made manifest by hemorrhage, edema, alteration in digestion, changes to the absorption and/or metabolism of nutrients, and mental changes and/or coma.
No animal species is immune to the acute toxic effects of aflatoxins; however, adult humans have a high tolerance for aflatoxin exposure and rarely succumb to acute aflatoxicosis.
Chronic, subclinical exposure does not lead to symptoms as dramatic as acute aflatoxicosis. Children, however, are particularly affected by aflatoxin exposure, which leads to stunted growth and delayed development. Chronic exposure also leads to a high risk of developing liver cancer, as aflatoxin metabolites can intercalate into DNA and alkylate the bases through its epoxide moiety. This is thought to cause mutations in the p53 gene, an important gene in preventing cell cycle progression when there are DNA mutations, or signaling apoptosis. These mutations seem to affect some base pair locations more than others — for example, the third base of codon 249 of the p53 gene appears to be more susceptible to aflatoxin-mediated mutations than nearby bases.
Moreover, aflatoxin B1 can permeate through the skin. Dermal exposure to this aflatoxin in particular environmental conditions can lead to serious health risks.
Some studies showed significant relationship between exposure of Aflatoxin B1 (4 mg/kg, single dose) with teratogenesis in hamsters.
Aflatoxins are recognized as the most important mycotoxins. They are synthesized by only a few Aspergillus species of which A. flavus and A. parasiticus are the most problematic. The expression of aflatoxin-related diseases is influenced by factors such as species, age, nutrition, sex, and the possibility of concurrent exposure to other toxins. The main target organ in mammals is the liver, so aflatoxicosis is primarily a hepatic disease. Conditions increasing the likelihood of aflatoxicosis in humans include limited availability of food, environmental conditions that favour mould growth on foodstuffs, and lack of regulatory systems for aflatoxin monitoring and control.
A. flavus and A. parasiticus are weedy molds that grow on a large number of substrates, in particular under high moisture conditions. Aflatoxins have been isolated from all major cereal crops, and from sources as diverse as peanut butter and marijuana. The staple commodities regularly contaminated with aflatoxins include cassava, chillies, corn, cotton seed, millet, peanuts, rice, sorghum, sunflower seeds, tree nuts, wheat, and a variety of spices intended for human or animal consumption. When processed, aflatoxins get into the general food supply where they have been found in both pet and human foods, as well as in feedstocks for agricultural animals. Aflatoxin transformation products are sometimes found in eggs, milk products and meat when animals are fed contaminated grains.
There are two principal techniques that have been used most often to detect levels of aflatoxin in humans.
The first method is measuring the AFB1-guanine adduct in the urine of subjects. The presence of this breakdown product indicates exposure to aflatoxin B1 in the past 24 hours. However, this technique measures only recent exposure, and, due to the half-life of this metabolite, the level of AFB1-guanine measured can vary from day to day, based on diet, and thus is not ideal for assessing long-term exposure.
Another technique that has been used is a measurement of the AFB1-albumin adduct level in the blood serum. This approach provides a more integrated measure of exposure over several weeks/months.
Aflatoxin has potential to lead to liver disease in dogs; however, not all dogs exposed to aflatoxin will develop liver disease. As with any toxic exposure, development of aflatoxicosis is a dose-related occurrence. Some dogs that develop liver disease will recover; those exposed to large doses for extended periods may not.
Low levels of aflatoxin exposure require continuous consumption for several weeks to months in order for signs of liver dysfunction to appear. Some articles have suggested the toxic level in dog food is 100–300 ppb and requires continuous exposure/consumption for a few weeks to months to develop aflatoxicosis. No information is available to suggest that recovered dogs will later succumb to an aflatoxin-induced disease.
Turkeys are extremely susceptible to aflatoxicosis. Recent studies have revealed that this is due to the efficient cytochrome P450 mediated metabolism of aflatoxin B1 in the liver of turkeys and deficient glutathione-S-transferase mediated detoxification. The mechanistic understanding of the susceptibility of turkeys to aflatoxin B1 is very relevant since turkeys are important from an agricultural standpoint.
There is no specific antidote for aflatoxicosis. Symptomatic and supportive care tailored to the severity of the liver disease may include intravenous fluids with dextrose, active vitamin K, B vitamins, and a restricted but high-quality protein diet with adequate carbohydrate content.
As a precautionary measure, both human and pet food recalls have occurred, casting a wide safety net to prevent exposure to potentially unsafe food. Recalled food products are subsequently sampled and tested for aflatoxin.
In 2005, Diamond Pet Foods discovered aflatoxin in a product manufactured at their facility in Gaston, South Carolina. Diamond voluntarily recalled in 23 states 19 products formulated with corn and manufactured in the Gaston facility. Testing of more than 2,700 finished product samples conducted by laboratories confirmed that only two date codes of two adult dog formulas with the "Best By" dates of April 3, April 4, April 5, and April 11 were potentially toxic.