ABSTRACT
174Trichothecene mycotoxins are a group of more than 300 toxins with only a few causing adverse effects in humans and animals. T-2 toxin, a trichothecene produced by Fusarium species, is prevalent worldwide in cereal crops, oil seeds, sugar beets, cereal-containing foods, and animal products such as eggs and milk. Similar to other trichothecenes, T-2 toxin is heat stable and cannot be destroyed by normal industrial processing. T-2 toxin is by far one of the most potent toxins among all known mycotoxins. The main toxic effect of T-2 toxin is the inhibition of protein synthesis, which arises from its direct binding to the 60S subunit of the 80S ribosome. This inhibition indirectly affects the synthesis of RNA and DNA. The effect of T-2 toxin in animals can be acute or chronic. Acute toxicity of T-2 toxin in animals results in weight loss, nausea, vomiting, abdominal pain and distention, diarrhea, bloody stools, dizziness, chills, inflammation, pharyngeal irritation, destruction of bone marrow, infertility, changes in brain neurochemistry, feed refusal, and lipid peroxidation. However, chronic T-2 toxicity can cause several adverse effects in multiple organs. These include hematological disorders such as neutropenia, thrombocytopenia, aplastic anemia, decreases in white blood cells count, and an increase in clotting time that might lead to coagulation problems. T-2 toxin ingestion for short periods of time causes edema and congestion in the gastrointestinal tract; however, feeding T-2 toxin for long periods cause intestinal necrosis to the epithelium and crypt cells of jejunum and ileum. T-2 toxin modulation of the immune system may be manifested by decreased activities of T and B lymphocytes, suppressed immunoglobulin production, and impaired macrophage activity. On the other hand, depending on the dose, route, and duration of administration, T-2 toxin can stimulate the immune system and superinduce the production of several cytokines. The inhibition of protein, RNA, and DNA synthesis is believed to be directly or indirectly responsible for immune suppression while the interference of the toxin with normal immune regulatory mechanisms might be responsible for immune stimulation. In vivo, T-2 toxin modulates the host resistance to certain bacteria. For example, it increases the host resistance to Listeria monocytogenes, while it decreases resistance to Salmonella typhimurium and has no apparent effect on host resistance to Mycobacterium bovis. The modulation of the immune system to several pathogens may predispose food animals to certain diseases that decrease productivity and might increase the period of shedding the microorganism. This might increase the susceptibility of animals and humans to the transmission of these pathogens. It is concluded that the health and welfare of the animals and to a lesser extent humans may be severely compromised by consumption of food and feeds contaminated with T-2 toxin. Therefore, it will be of great interest to genetically engineer crops resistant to Fusarium and to find methods to detoxify these toxins.
