Welcome to my blog ‘Zearalenone: What You Need To Know’.
You may also like to read my blog, Mould Illness: A UK Functional Medicine Approach.
What Is Zearalenone?
Zearalenone (ZEA), also known as F-2 toxin, is a mycotoxin produced by fungi of the genus Fusarium, widely exists in animal feed and human food.
The structure of zearalenone is similar to estrogen, so it mainly has estrogenic effects on various organisms. Products contaminated with zearalenone can pose risks to animals and humans.
Zearalenone is one of the top five agriculturally important and of greatest concern mycotoxins. Its toxicity is mainly manifested in the following aspects (source):
- Reproductive toxicity.
Zearalenone Toxicity In Humans
The structure of zearalenone is similar to estrogen, so it mainly has estrogenic effects on various organisms. Therefore, it is imperative to carry out toxicological research on zearalenone and evaluate its risk to human health. (source)
When the toxin is intaken by mammals, the ketone group at the C-8′ position of ZEA may reduce and transform to α- and β-zearalenol (zearalenol, ZOL), both of which have estrogen hormone-like structures. These substances may bind to human estrogen receptors (ER-α and ER-β) in competition with 17-β-estradiol. Thus, ZEA, α-zearalenol, and β-zearalenol have estrogenic activity. Previous studies have shown that the estrogenic activity of α-zearalenol is three times that of ZEA, while the estrogenic activity of β-zearalenol is similar to ZEA. Zearalenone and its derivatives interact with animal estrogen receptors. They are defined as estrogenic mycotoxins. Their toxicokinetics, toxicity, and estrogenic effects have attracted extensive attention. (source)
With more attention paid to the intestinal environment and chronic metabolic diseases in recent years, molecular biology methods were applied to explore ZEA’s impact on intestinal health and endocrine homeostasis. It is found that ZEA may damage intestinal health and interfere with endocrine stability. This state leads to a series of metabolic disorders, and the potential effects of long-term low-dose exposure to zearalenone on the body need special attention.(source)
Liver Toxicity And Zearalenone
The liver is another target organ for ZEA toxicity.
ZEA may change the activity of liver enzymes, the degree of lipid peroxidation, the content of liver protein, the antioxidant capacity, and the inflammatory response, which leads to hepatotoxicity. Additionally, ZEA may cause DNA damage to hepatocytes and severe damage to liver function. The liver damage extents can be assessed by testing specific liver enzymes (source):
Gut Health And Zearalenone
In addition to basic toxicological research, mycotoxins and gut health have received increasing attention in recent years. When humans and animals ingest mycotoxins, the gut is the first to be affected. Mainly, the toxin may affect gut histomorphology and gut microbes. The intestinal barrier refers to the physical, chemical, biological, and immune barriers. ZEA may destroy these barriers, thus resulting in decreased intestinal resistance to toxins and affecting the immune function. (source)
What foods are high in Zearalenone?
ZEA mainly exists in moldy food and crops. It is less sensitive to environmental changes and heat treatment, and thus remains stable during food storage and processing. ZEA mainly contaminates grains, such as corn, wheat, rice, barley, sorghum, soybean, oat, and their products; animal milk may be contaminated when their feedstuff has a high ZEA concentration. (source)
Additionally, poultry inevitably contains Zearalenone in vivo when fed with feedstuff and vegetable oils that contain or contact with mold-contaminated ingredients. (source)
Several studies have found that ZEA is widely distributed in animal tissues and slowly scavenged. The liver is the main organ for ZEA deposition. Besides, ZEA distributes to organs or tissues, including the kidney, intestine, adipose tissue, and reproductive organs (uterus, testis, and ovary) (source)
How Do You Treat Zearalenone?
The major organs involved in the biotransformation of ZEA are the liver and gut.
After the phase-I metabolism, the ZEA and its metabolites bind to glucuronic acid in phase-II metabolism. In this step, the toxin and its metabolites are conjugated by uridine diphosphate glucuronyltransferase. Thereby, it forms modified or masked metabolites such as derivatives conjugated with glucose, sulfate, or glucuronide. (source)
Therefore supporting sulfation by taking epsom salt baths regularly may be helpful.
Part of ZEA and its metabolites, and most of its conjugated compounds produced by phase-II metabolism, are excreted in urine or feces. (source)
Bile excretion and entero-hepatic circulation (EHC) are the major ZEA excretion and reabsorption processes in most mammals. ZEA-glucuronide derivations are abundantly collected in bile, reabsorbed, and metabolized by intestinal mucosal cells. Again, the toxins enter the portal vein blood, liver, and systemic circulation, where ZOL with high estrogenic activity may be formed. The reabsorption process affects the metabolized and endocrine balance, increasing ZEA’s retention time, prolonging the duration of toxic effects, and delaying its elimination. (source)
Some yeast and Lactobacillus strains are cytologically compatible with ZEA, thus adsorbing ZEA and reducing its bioavailability. Additionally, microorganisms such as Bacillus subtilis were found to change the molecular structure of ZEA during their metabolic processes so that the estrogenic effect of ZEA can be reduced. (source)
The combination of four probiotics, Bacillus subtilis, Lactobacillus casein, Candida utilis, and Aspergillus oryzae antagonized the toxicity of ZEA by alleviating intestinal inflammation and apoptosis. (source)
Further studies are required on the in vivo detoxification of ZEA by natural products and probiotics. (source)