Mycotoxins are toxic secondary metabolites produced naturally by various species of fungi. These compounds are not required for the fungus’s survival but pose significant risks when they contaminate human food and animal feed. Trichothecene mycotoxins are a major family known for their potent biological activity and widespread presence. Their prevalence in cereal crops makes them a serious concern for food security and public health worldwide.
Classification and Common Types
Trichothecenes share a common core chemical structure: a tetracyclic sesquiterpenoid ring system. The presence of the epoxide group in this structure is fundamental to the toxicity of the entire class. Classification is based on the substitution patterns of functional groups attached to this core.
The most common trichothecenes are divided into two main categories: Type A and Type B. Type A trichothecenes, such as T-2 toxin and diacetoxyscirpenol (DAS), lack a carbonyl group at the C-8 position and are generally the most acutely potent toxins. T-2 toxin is known for its high toxicity.
Type B trichothecenes, including Deoxynivalenol (DON) and Nivalenol (NIV), are distinguished by the presence of a carbonyl group at the C-8 position. DON is the most frequently detected trichothecene in agricultural products globally, though it is less acutely toxic than T-2 toxin.
Primary Sources of Exposure
Exposure occurs primarily through the consumption of contaminated cereal grains. Fungi from the Fusarium genus, especially F. graminearum and F. culmorum, are the main producers of Type B toxins like DON. These fungi infect crops such as wheat, barley, maize, and oats while growing in the field, particularly during cool, wet weather.
Contamination begins pre-harvest, and the toxins persist into finished food products because trichothecenes are highly stable and resist degradation by heat, surviving conventional processing like baking and milling. When grains are milled, the toxin is redistributed. DON concentrations are often highest in the outer layers of the grain, leading to elevated levels in products like bran and milling by-products.
These by-products enter the animal feed supply, creating a secondary exposure route for humans through the consumption of livestock products. Exposure can also occur through inhalation from indoor molds like Stachybotrys chartarum, which produces macrocyclic trichothecenes in damp environments.
Cellular Mechanism of Toxicity
The effects of trichothecenes stem from their rapid interference with cellular machinery. The primary mechanism of action involves the inhibition of protein synthesis in eukaryotic cells. Trichothecene molecules achieve this by non-covalently binding to the peptidyl transferase center of the 60S subunit of the ribosome.
By binding to this site, the toxins halt the elongation phase of the protein chain. This shutdown of protein production severely affects rapidly dividing cells, including those lining the gastrointestinal tract, skin, bone marrow, and immune system organs.
This ribosomal binding also triggers a cellular defense mechanism known as the “ribotoxic stress response.” This response activates specific signal transduction pathways, which can lead to inflammation and ultimately programmed cell death (apoptosis) in the affected cells.
Acute and Chronic Health Effects
The health consequences of trichothecene exposure vary based on the specific toxin, dose, and duration. Acute exposure, often linked to Type B toxins like Deoxynivalenol (DON), primarily affects the digestive system. DON has a potent emetic effect, earning it the nickname “Vomitoxin.”
Ingestion of contaminated food can quickly cause symptoms like nausea, vomiting, abdominal pain, and diarrhea. This emetic response is mediated by the toxin acting on the central nervous system and triggering the release of gut hormones.
Exposure to the more potent Type A toxins, particularly T-2 toxin, has been linked to severe poisoning events such as Alimentary Toxic Aleukia (ATA). This syndrome involves the progressive destruction of blood-forming tissues, leading to leukopenia (a severe reduction in white blood cells). ATA causes necrosis and hemorrhagic lesions throughout the digestive tract, fever, and dermal inflammation, and can be fatal.
Chronic, low-level exposure is mainly associated with immunosuppression, increasing susceptibility to infectious diseases. These toxins suppress the immune system by attacking rapidly proliferating cells in lymphoid organs. Contact with T-2 toxin can also cause severe local irritation, including skin inflammation, blistering upon dermal exposure, and respiratory irritation when inhaled.
Strategies for Minimizing Exposure
Efforts to control trichothecene exposure are implemented through industry regulation and individual food handling. Regulatory bodies, such as the European Union and the U.S. Food and Drug Administration, set maximum limits for DON and other trichothecenes in food and feed. For example, regulations set specific maximum thresholds for DON, T-2, and HT-2 toxins in various cereal products.
Consumers can reduce dietary exposure at home. Since trichothecenes are heat-stable and do not break down during standard cooking, prevention focuses on minimizing mold presence in the food supply. Grains, flour, and nuts should be stored in cool, dry conditions and airtight containers to prevent moisture accumulation and fungal growth.
Consumers should regularly inspect stored food items and promptly discard any with visible signs of mold, discoloration, or damage. Simple methods like hand-sorting and washing can help reduce contamination in high-risk foods, as mycotoxins are often concentrated in visibly damaged kernels. Consulting professional services to remediate household mold issues, especially from Stachybotrys chartarum, helps eliminate potential inhalation exposure.