Using milk thistle to reduce liver damage from mycotoxins

Mycotoxins are a constant problem in cereals causing economic losses to the global animal industry. Mycotoxins are produced by filamentous fungi varying widely in their chemical and biological characteristics and effects on animals. Among the various mycotoxins, aflatoxins, and more specifically aflatoxin B1, is one of the most problematic because it affects maize, one of the major staple ingredients in animal diets worldwide. Of course, in nature, mycotoxins mostly occur in combinations, but even with singly contaminated ingredients, the nature of animal feeds leads to the concurrent presence of multiple mycotoxins, coming from the different ingredients. The separation of mycotoxins in polar and non-polar, however, simplifies their management. For example, aflatoxins (polar) are easily addressed by the inclusion of an adsorbent (like bentonite, for example). The same ingredient adsorbs not only aflatoxins, but also other mycotoxins, like zearalenone, ochratoxin A, and T-2 toxin, albeit at reduced efficiency.

Products limited to work in gut

Certainly, anti-mycotoxin agents are effective only while the feed is being digested, that is, while the feed remains in the lumen of the gastrointestinal tract. Anti-mycotoxin agents are not absorbed by the animal, whereas non-adsorbed mycotoxins are; leading to the need for further detoxification within the organism. A part of the mycotoxins might enter the organism despite the use of an anti-mycotoxin agent in feed due to the fact that no product is 100% effective, not all mycotoxins are affected similarly by a single product, non-polar mycotoxins might not be inactivated if only a polar agent is used, and vice versa and lastly, high contamination might render the normal dosage inadequate. This is often seen as being the most common cause, In other words, some mycotoxins in the feed can still enter the animal. The exact effects on animal health and performance will depend, of course, on the initial contamination levels in the feed and on the constitution of the liver.

Mycotoxins are detoxified in the liver

Absorbed mycotoxins, like all toxins, are detoxified in the liver, assuming the liver is not overpowered and in good health. There, the detoxification is a two-phase biotransformation process. Phase 1 is the addition of a functional group (e.g., hydroxyl or carboxyl group) to the toxin. This causes the toxin to become more reactive with other compounds so that it may become even more polar in the next phase. Phase 2 includes the modified toxin is now conjugated with endogenous substrates (e.g., glucuronic acid or sulphate). This transforms the toxin to a highly polar compound that can be excreted easily through the bile and urine.

Among the various mycotoxins, aflatoxins, and more specifically aflatoxin B1, is one of the most problematic because it affects maize, one of the major staple ingredients in animal diets worldwide.

Failure of the above biotransformation leads to hepatotoxicity and consequently to liver damage, which causes significant loss of performance, health problems, and even death.

Mycotoxins and liver damage

Even short-term exposure to mycotoxins suffices to cause significant liver damage and loss of performance. In a study (Meissonnier, 2007), pigs were given 385, 867, or 1807 μg aflatoxin B1/kg feed for four weeks. Pigs receiving the highest level of aflatoxin developed clear signs of aflatoxicosis: hepatic dysfunction and decrease in weight gain. Also, the pigs exposed to the lower levels of mycotoxins showed clear signs of impaired metabolism and biotransformation.

Additionally, mycotoxins and particularly aflatoxins inhibit the major hepatic biotransformation enzymes. This has significant consequences in veterinary medication applications as animals become unable to clear medications from their system – and of course, other toxins.

Silimarin: a natural liver protector

Milk thistle is an herb plant native to the Mediterranean and North African regions. The seeds of this plant contain a mixture of flavonolignans known as silymarin. Today, silymarin is used in human medicine for oral treatment of toxin liver damage and therapy of chronic inflammatory liver diseases. It is believed that the significant hepatoprotective activity of silymarin is due to its multi-factor actions including:  binding to cell membranes to suppress penetration of toxins into hepatic cells, increasing superoxide dismutase activity, increasing glutathione tissue concentration, inhibiting lipid peroxidation, and enhancing hepatocyte protein synthesis.

The hepatoprotective activity of silymarin can thus be explained based on its strong antioxidant, immunostimulating, anti-inflammatory, and regenerating properties.

Silymarin and broiler aflatoxicosis

Silymarin has been also tested against aflatoxicosis in broilers (Tedesco, 2004). In that study, 14-day-old male broilers were randomly allotted to 3 groups: A. basal diet; B. basal diet plus 0.8 mg/kg aflatoxin B1; C. basal diet and 0.8 mg/kg aflatoxin B1 plus silymarin at 600 mg/kg body weight. Results indicated that weight gain and feed intake were lower in aflatoxin-treated birds compared to control (P < 0.05). Interestingly, however, silymarin supplementation (group C) improved (P<0.05) both weight gain and feed intake compared to birds receiving aflatoxin alone (group b), and this improvement restored performance to the level of control birds (group a). serum biochemistry showed no meaningful differences among groups, whereas no treatment differences were noted on liver weight.>

Silymarin protects against hepatotoxic effects of feed aflatoxins

In conclusion, these results suggest that silymarin provides significant protection against the hepatotoxic effects of feed aflatoxins and restores performance in affected broilers. An anti-mycotoxin agent in combination with a hepatoprotector is highly advisable in the event of mycotoxin contaminated feed, specially feed containing more than one mycotoxin as it will on one hand adsorb the mycotoxins, and on the other protect the liver from the effects of non-adsorbed mycotoxins.