Trichothecenes

What Are Trichothecenes

Trichothecene mycotoxins are a large group  with over 200 chemically related toxins, but only a few cause significant toxicity to humans.  These chemically related toxins  are produced by a variety of mold species such as Fusarium (the main culprit), Myrothecium, Stachybotrys, Trichoderma, and Trichothecium. Some of them occur commonly in the animal and human food supply as well as in water-damaged buildings. The most common trichothecene in food is deoxynivalenol (DON). Tricothecenes such as 3-acetyl DON, T-2 toxin, and nivalenol are also found in food. T-2 is considered to be one of the most hazardous and because both T-2 and DON are frequent contaminants of food, they are of great concern and are currently getting more attention.

The trichothecenes may be large in number, but they are small amphipathic (polar and nonpolar portions) molecules that can easily  move across cell membranes. They are sesquiterpenoid mycotoxins with a 12,13-epoxy-trichothec-9-ene skeleton. As mentioned, most have been isolate from Fusarium genus. They range from being slightly hydrophilic such as deoxynivalenol (DON) to moderately hydrophobic such as HT-2 and T-2. and include T-2 toxin(T-2), HT-2 toxin (HT-2), deoxynivalenol (DON), Diacetoxyscirpenol (DAS), Fusarenone-X (FUS-X), Nivalenol (NIV), diacetylnivalenol (DAS) and neosolaniol. Mycotoxins of the Fusarium species are generally of two types: (1) the nonestrogenic trichothecenes such as DON, NIV, T-2, and DAS; (2) the mycoestrogens, including Zearalenone (ZEA or ZEN) . Zearalenone  is a nonsteroidal, estrogenic mycotoxin and has been shown to be able to bind competitively to estrogen receptors. It is known as a serious endrocrine disruptor. The black mold Stachybotrys chartarum is also known to produce trichothecenes such as Satratoxin-G (SG) and T-2.

The genus Fusarium is common in soil, marine and river environments as well as on plants all over the world. F. species are some of the most problematic molds known in the northern temperate regions of the world. They are responsible for many plant diseases and they can produce potent mycotoxins. Fusarium mycotoxins are commonly found on grains. Besides ingestion, Fusarium mycotoxins can also gain access to the body by inhalation. The most important Fusarium food mycotoxins are the families of trichothecenes, and fumonisins.

Toxins from Fusarium in food largely depends on environmental conditions, such as temperature and humidity. This means Fusarium caused toxin contamination can not be avoided completely. Therefore, exposure to toxins from this mold is a permanent health risk for both humans and farm animals.

Fusarium has been noted in some research papers to grow like crazy after application of glyphosate (RoundUp). See research here.

Masked Trichothecenes

Trichothecene glycosides have been isolated from Fusarium-infected plant material. Trichothecene glycosides have been called masked mycotoxins because they may escape extraction or detection by methods that are commonly used to monitor mycotoxin contamination of food and feed

Where Are Trichothecenes Found

Trichothecene is most common associated with wheat, barley, oats and corn. T-2 toxin and DON have a high toxicity and are frequently found contaminating food. Trichothecenes are also associated with water-damaged buildings.

Health Effects Of Trichothecenes

They can affect people or animals through the usual methods of ingestion, eye contact, skin contact and inhalation. Trichothecenes are small molecules and can move passively across cell membranes. They are easily absorbed by the skin and the gastrointestinal system, allowing for immediate effect on tissues with rapid cell turnover. Oral toxicity of these trichothecenes to an organism is considerably influenced by the organism’s intestinal microflora. Reactions of the skin, or intestinal mucosa are provoked rapidly after direct contact through dermal application or ingestion of the compound.

Trichothecenes cause mitochondrial dysfunction, which is largely associated with the oxidative stress. Oxidative stress mediated by trichothecenes and their related toxicities pose a great risk to human health. Trichothecenes generate free radicals, including reactive oxygen species (ROS), which induces lipid peroxidation, decreases levels of antioxidant enzymes, and ultimately lead to apoptosis.

Oxidative stress changes the antioxidant state of the cells, reducing intracellular reduced glutathione (GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD), and catalase (CAT) in the body.

DNA damage is an early event associated with the generation of ROS and lipid peroxidation. Some signaling pathways, including MAPK, JAK/STAT, and NF-κB, are subsequently induced by oxidative stress, and the caspase-mediated apoptosis pathways are also activated.

One of the main issues noted by in large animal production facitlities is the issue of mycotoxins in the food, and tricothecenes in particular, increasing animal susceptibility to pathogens and disease. This has also been noted in human toxicity to the T-2 toxin trichothecene. People who are sick from exposure to water-damaged buildings often have multiple aflictions and have trouble recovering from infectious disease.

 

Health Effects of Trichothecenes In General

• Inhibition of proetin synthesis - causes general cytoxic effects
• Depressed intestinal function - can cause intestinal lining to become more permeable
• Depressed immune funcction - Trichothecenes are highly immunotoxic
• Neurotoxicity - can cause blood-brain-barrier to become more permeable
• Cytotoxicity
• Oxidative stress
• Carinogenic
• Cardiotoxic
• Skin toxicity
• Bone marrow damage
• Liver toxicity
• Reproductive toxicty and teratogenic effects
• Associated with Kashin-Beck disease and Alimentary toxic Aleukia
• Hematologic (blood) toxicity
• See specific effects of indiviudal trichothecenes below.

From military: Diagnosis of an acute attack of trichothecene mycotoxin depends on clinical observations and identification of the toxin from biological and environmental samples. Initial laboratory studies are nonspecific. Elevations of serum creatinine, potassium, and phosphorus may occur, as well as abnormalities of coagulation parameters. An initial rise in absolute neutrophils can be observed. Leukopenia, thrombocytopenia, and anemia may occur 2-4 weeks following initial exposure.

Trichothecenes Affect Mammals Differently: Poultry are more affected by trichothecenes than ruminants and pigs are the most affected of the farm animals. Ruminants are most likely protected by the microbes that live in their rumen.

Chronic Toxicty Of Trichothecenes Due In Part To Oxidative Stress

Studies have shown that oxidative stress is a crucial toxic effect of trichothecenes that causes DNA cleavage and apoptosis. Oxidative stress appears to be a mechanism of toxicity with other mycotoxins also. These mycotoxins activate a rapid production of reactive oxygen species (ROS), and decreased intracellular reduced glutathione. They have been shown to increase lipid peroxidation, and cause mitochondrial dysfunction due largely to oxidative stress. Ultimately they cause apoptosis. They reduce the activity of antioxidant enzymes and it has been shown that antioxidant supplements can be beneficial against DON-induced protein and lipid peroxidation.

Immunotoxicity

Recent studies have revealed that an “immune evasion” mechanism is involved in trichothecene immunotoxicity, through which the toxins can escape host and vaccine immune resistance, that allows pathogens to escape host defenses. Some trichothecenes, especially macrocyclic trichothecenes, also potently kill cancer cells.

Evidence has shown that trichothecenes significantly downregulate IFN-γ expression in pigs and rats, thereby reducing the host resistance to viruses and their repairing ability. Type B trichothecenes deoxynivalenol (DON) reduces IFN-γ gene expression in pigs and reduces their immune response to vaccine ovalbumin. The effect of the trichothecenes may modulate the immune system and allow pathogens to escape the usual host immune response.

 

A Look At The Trichothecenes Deoxynivalenol, T-2 Toxin and Satratoxin-G

 

Deoxynivalenol(DON)

DON has a negative charge. In research on water-damaged buildings it was found to be associated with  Acremonium sp., Aspergillus versicolor, and Aureobasidium sp. in some of the samples removed.

 

Where You Might Come In Contact With The Trichothecene Deoxynivalenol(DON)

In grains, the most common Fusarium molds to make the toxin DON are Fusarium graminearum and F. culmorum. DON is also called vomitoxin, and it is found in both food and water-damaged buildings. It is the most comon trichothecene contaminant of cereal grains in many countries including Canada and the United States.

 

In Food

DON is one of the most prevalent and hazardous food-associated mycotoxins, particularly in cereals and cereal-derived products. Deoxynivalenol is a common contaminant in wheat, barley and corn. In the US, 73% and 92% of wheat and corn samples, respectively, were found positive for DON [Canady R. & others, 2001] In Europe, a large-scale collaborative study conducted on more than 40,000 food samples has shown that DON was present in 57% of all samples, with a percentage of positive samples varying depending of the country. [Schothorst R.C., 2004] Fusarium graminearum is the leading cause of DON contamination in maize and small grains in the United States. The fungus causes a disease of wheat and barley known as Fusarium head blight and a disease of corn known as Gibberella ear rot. Infected wheat spikelets exhibit premature bleaching as the pathogen progresses within the head and the developing grain becomes contaminated with DON. Maize ears infested with F. graminearum are often covered with a pinkish fungal mycelium as the maturing kernels become contaminated with DON. In addition,  animal derivatives of DON may be present in food originated from animal tissues and blood or  milk, however there is little reserach on this. It appears that it is in the milk of dairy animals but at low concentrations generally. The amount of DON metabolites has not been considered in the regulatory limits fixed by food agencies for DON due to the lack of data regarding its absorption and toxicity.

In Water-Damaged Buildings

Although DON is not one of the more common mycotoxins found in indoor air, in a 2000 research study 19% of samples contained trichothecenes and DON was one of them.

 

Health Effects of Deoxynivalenol (DON) - type of trichothecene

Most of the research on DON is around ingestion of DON in food. That data is still helpful if you are dealing with it in a moldy building.

Acute toxicity

Common symptoms are diarrhea, vomitting, anorexia, gastro-intestinal inflammation, depression of intestinal function - reduced absorption of nutrients, depression of immune system - increased susceptiblitiy to infection and disease. Related to Kashin-Beck disease.

The World Health Organization mentions a report of children in a U.S. school (DON is not regulated in U.S.) who ate DON in burritos for lunch and and the most predominant symptoms were:

• abdominal cramps 88%
• vomiting 62%
• headache 62%
• nausea 39%

Chronic toxicity

Deoxynivalenol has been shown to enhance the inflammatory response to food-borne bacterial pathogens. (The endotoxins from gram negative bacteria sensitize macrophages, amplifying the innate immune response.) DON has also been shown to to be immunotoxic to animals.

The ingestion of DON has been associated with alterations of the intestinal, immune and nervous systems, thus leading, in cases of acute exposure, to illnesses characterized by vomiting, anorexia, abdominal pain, diarrhea, malnutrition, headache and dizziness.

In 1987 several thousand people in India were poisoned by tricothecenes. 97 reported feeling abdominal pain within 15 min to 1 hour after eating food made with bread that was later found to contain tricothecenes. Other symptoms included throat irritation (63%), diarrhea (39%), vomiting (7%), blood in stools (5%) and facial rash (2%). Increased respiratory tract infections were reported in children who ate the bread for more than a week. The illnesses disappeared when the flour was found to be contaminated and they stopped eating it. Samples of flours and wheat in the local markets contained DON (11/17 had toxin levels of 0.346 to 8.38 μg/g), nivalenol (2/19 had levels of 0.03 to 0.1 μg/g), T-2 toxin (4/19 had levels of 0.55 to 4 μg/g), and 3-acetyl DON (4/19 had levels of 0.6 to 2.4 μg/g), but were negative for aflatoxins and ergot alkaloids (Bhat and others 1989).

Chronic exposure to DON contaminated foods may damage the gut barrier and cause intestinal hyperpermeability which in turn can trigger a chronic inflammatory response at the level of the gut wall. In chickens DON at concentrations ranging from 1 to 7 mg/kg diet significantly alters several key functions of the intestinal tract including decreasing villus surface area available for absorption and altering the permeability of the intestinal tract.

Deoxynivalenol is resistant to high temperature (up to 350 °C), thereby making it stable during processing and cooking, leading to its persistence throughout the food chain. However DON is altered by gut microbes.

Grain crops are commonly contaminated with DON and animal diets consist mainly of grains in industrialized countries. It can be assumed that animals consuming grains are frequently exposed to DON-contaminated feeds. A variety of methods are used to decrease the toxic effects of DON. This includes pre-harvest, post-harvest and storage methods to decrease mold. However, additional approaches by the farmer can be taken. Farmers have tried adding adsorbent materials to the feed to bind the mycotoxins in the gastrointestinal tract and reduce absorption of the mycotoxin. Some research shows use of adsorbents can decrease many mycotoxins but generally the efficacy against trichothecenes is negligible. One method that has been shown to be beneficial is the use of gut bugs. These are also called beneficial micro-organisms or probiotics. Deoxynivalenol  has been completely transformed to de-epoxy DON by ruminal and intestinal microflora. Eubacterium BBSH 797 is one bacteria that has been shown to degrade DON and stop the effects of DON on animals.
(Awad, Bohm , Zentek, 2010)

Inhibition of protein synthesis is thought to be the fundamental mechanism of trichothecene toxicity. The epoxide group is necessary for the inhibition of protein biosynthesis. Two mechanisms leading to destruction of the epoxide group of trichothecenes have been reported: reductive de-epoxidation leading to olefin and hydrolytic de-epoxidation generating two vicinal hydroxyls. The possibility of nucleophilic attack of the epoxide group by thiols in plants was suggested (Subramanian 2002) but not supported by data.

Research has shown bacteria in the digestive system of animals are able to reduce the epoxide group of trichothecenes, generating 9,12-diene derivatives. The structure of the product of the de-epoxidation of DON was first examined in the 1980s. (Yoshizawa et al. 1983; King et al. 1984). Since then, the de-epoxidation of trichothecenes by mixed populations of ruminal and intestinal bacteria has been repetatively documented (Yoshizawa et al. 1985, Swanson et al. 1987a; Lake et al. 1987; Worrell et al. 1989, He et al. 1993; Kollarczik et al. 1994). Negative results reported by some authors (He et al. 1992; Swanson et al. 1987a, b; Munger et al. 1987) may be accounted for by the intestinal or ruminal microbes having not been previously exposed to trichothecenes and therefore having lacked the necessary adaptation. In support of this explanation, Hedman and Pettersson (1997) reported that neither DON nor nivalenol was detoxified in pig feces unless the pigs were fed with a diet containing trichothecenes. The experiments confirming this observation for chickens are described in a recent patent application by Zhou et al. (2010). Patents have been taken out on bacteria of the Bacillus spp. and Eubacterium sp for commercial use to lower DON in animal feed. Other genus's that de-epoxidize DON in research are Clostridiales, Anaerofilum sp., and Collinsella sp. For more data on DON and methods to alter and detoxify it I suggest this research article "Biological detoxification of the mycotoxin deoxynivalenol and its use in genetically engineered crops and feed additives".

Research shows that DON stimulates proinflammatory cytokines in the gut. IL-1B, IL-6, IL-8 TNF-alpha, IFN-gama, IL-10 is increased significantly.

Reproductive toxicity of animals induced by DON was shown to be inhibited by resveratrol in vitro.

 

Possible Treatments For DON Exposure

Resveratrol: Reproductive toxicity of animals induced by DON was shown to be inhibited by resveratrol in vitro.

Gut Flora: DON has been shown to be almost completely removed by protozoa in Cows rumen. Additionally there are bacterial flora that appear to lower DON that include Bacillus spp. and Eubacterium sp that have been used in animal feed. Other genus's that de-epoxidize DON in research are Clostridiales, Anaerofilum sp., and Collinsella sp.

Antioxidants: Tricothecenes are shown to reduce the activity of antioxidant enzymes and it has been shown that antioxidant supplements can be beneficial against DON-induced protein and lipid peroxidation.

 

T-2

T-2 has a positive charge. In research on water-damaged buildings it was found to be associated with  Aspergillus sp., and Chaetonium in some samples. Fusarium spp. are the mold that usually makes T-2. It has been shown to be made by Fusarium moniliforme, F. equiseti, F. culmorum, F. solani, F. avenaceum, F. roseum, F. nivale Fusarium tricinctum, F. poae, F. sporotrichiella, F. graminearum.

 

Where You Might Come In Contact With The Trichothecene T-2

T-2 toxin has been found in water-damaged buildings. This toxin may also contaminate small grains including wheat, corn, barley, rice, soybeans and particularly oats . T-2 is a problem in grain contamination in Europe, especially in thye Nordic coutnries. A comparison of grain commodities shows that feed and food products that contain oats are often morecontaminated with high levels of T-2 than other grains.  In the 1940s in the Oregnburg District of the USSR, 10% of the population died from what they suspect was mass food poisoning from fusarium mold growing on grain that created T-2 toxin. T-2 toxin has been implicated as part of the alleged chemical warfare agent ‘yellow rain’ in Southeast Asia. Eyewitnesses claimed low flying aircraft released a yellow, oily liquid over Southeast Asian populations. T-2 is also claimed to be the cause of  Gulf War Syndrome. (It would be nice if the classified documents around this scenario would be unclassified so people would know what the likely cause of their affliction is.)

As with other mycotoxins, indirect exposure from contaminated objects and surfaces that are not property decontaminated has been shown to spread T-2 to other individuals.

 

Health Effects of T-2

T-2 toxin is known to be one of the most toxic trichothecene mycotoxins. T-2 has been shown to penetrate the lungs easily as well as be topically absorbed  and  has been shown to cause rapid response to skin contact and ingestion. In addition to being highly toxic by itself, it also exacerbates the effect of  ionizing radiation.

T-2 toxin causes a fatal disease of humans known as alimentary toxic aleukia (ATA); a disease that was particularly problematic in Russia in the 1940s during the fusarium mold outbreak on their grains. Symptoms of ATA in humans include skin pain, vomiting, diarrhea, complete degeneration of bone marrow, and eventually death. Additionaly symptoms noted with T-2 toxicity are dizziness, chills, abdominal pain, skin necrosis, abortion, reduced white blood cells (which decreases antibodies), breakdown or red blood cells, inhibition of protein synthesis, and allograft rejection.

Broiler chickens fed low doses of T-2 toxin may demonstrate symptoms of weight loss, feather malformation, and yellowing of the beak and legs.

T2 is produced predominantly by Fusarium sporotrichioïdes and F. langsethiae. Exposure to T-2 toxin is associated with low white blood cell counts and cell depletion in lymphoid organs as well as inhibition of red blood cell formation in bone marrow and the spleen. Furthermore, T-2 toxin reduces proliferation of the white blood cells called lymphocytes and it disturbs the maturation process of dendritic cells (an antigen presenting cell).

After hearing all these various ways that T2 depresses the immune system, it is no surprise that exposure to T-2 suppresses immune response to systemic bacterial infections such as Salmonella typhimurium, Listeria monocytogenes, Mycobacterium bovis, and Babesia microti. Respiratory immune defences are also compromised by T-2 exposure. T2 also has been shown to decrease viral resistance. If you have read much research on mycotoxins, you will already know that immunotoxicity is common amongst mycotoxins.

The acute affect of T-2 on rabbits was gastroenteritis, damage of digestive cells, liver cells, and white blood cells as well as adrenal cortex cells and the blone marrow. The subacute affect on rabbits was stomach inflammation, emaciation, and hypertrophy of the adrenal cortex.

The chronic affect in animals seems to involve loss of weight,  decreased red blood cell and white blood cell counts, decreased glucose levels and detrimental changes to the digestive tract. It has also been noted that it increases the infection rate of animals.

T-2 has been shown to inhibit protein synthesis, interfere with metabolism of membrane phospholipids and increases liver and brain LPO. It also suppresses glutathione-S-tranferase, increase reactive oxygen species generation, depletes glutathione,

 

Possible Treatments For T-2 Exposure

Chemically, the T-2 toxin is insoluble in water but soluble in acetone, ethyl acetate, chloroform, ethanol, methanol and propylene glycol.  Inactivation is said to be achieved by heating it to 900°F for 10 min or 500°F for 30 min. There are bacteria and fungi that can also inactivate it by altering its chemical structure.

People who live in areas with trichothecene produced by fusarium and have sensitivity to trichothecenes, feel like air filters can help remove it from the air and that below-freezing temperatures as well as snow may decrease its presence in the air. Although there are no studies on this that I know of, getting first hand information from people like this is very useful.

The military has had experience with T-2 and has put out some data on how to deal with exposure. They have a cream they use (Reactive Skin Decontamination Lotion ) which is not shared with you or me as it is considered a national secret. Here is what has been shared with the medical community: Remove all clothing, and clean and scrub the patient's entire skin surface with soap and water. Washing the contaminated area of the skin within 6 hours post exposure can remove 80-98% of the toxin and has been demonstrated to prevent skin lesions and death in experimental animals.(This is true with other mycotoxins often too and is why sensitive people should always wash their body, hair, wash eyes if irritated and gargle as well as rinse their nose after exposure. It can help people who are really sensitive to mycotoxins in general.) They claim the proposed mechanism of action is neutralization of traditional chemical warfare agents by a combination of physical removal and nucleophilic breakdown, which renders the original toxic substance nontoxic. It is suggested that clothing be contained and disposed of. (Clothing of sensitive people who are exposed to usual mycotoxins in water-damaged buildings should always be washed and I suggest with a good hydrogen peroxide bleach.)

The T-2 toxin is able to undergo microbial transformation into its deepoxylated form in the intestine which is very important in toxin-reduction. Both bacteria and enzymes are being used to prevent and treat T-2 toxicity in farm animals. Additionally there are a number of antioxidants and other supplements that can be beneficial. There is additional information on treatment for T-2 toxin here.

 

Trichothecene Treatment In General

Trichothecenes are very stable mycotoxins.  Chemical treatments have been used effectively in food. Several types of microbial bioconversions of trichothecenes have also been reported  including oxygenation, acetylation  deacetylation, oxidation, deepoxidation, and epimerization. There has been complete loss of toxicity of the trichothecenes using deepoxidation, and reduction of their toxicity using acetylation, and oxidation of the food items.  Changes to the C-3 position and the epoxide have the greatest impact on toxicity. Microbes or enzymes that degrade or detoxify mycotoxins such as the trichothecenes are being studied, and used as additives in animal feeds.

It is possible that all the trichothecenes may be altered by gut bacteria but the research is in its early stages. Glucomannans look useful as do antioxidants and supporting the biotransformation system as mentioned above and it also appears that charcoal may be the binder of choice according to recent evidence. This all needs additional research though.

Antioxidants Used For Various Trichothecene Toxicity

Research on Glucomannans

Comp Biochem Physiol C Toxicol Pharmacol. 2003 Jul;135C(3):337-43.

Protective effect of modified glucomannans against aurofusarin-induced changes in quail egg and embryo.

Dvorska JE1, Surai PF, Speake BK, Sparks NH.

Abstract
The aim of this study was to evaluate effects of modified glucomannans (Mycosorb) on egg yolk and liver of the day-old quail after aurofusarin inclusion in the maternal diet. Fifty-four 45-day-old Japanese quail were divided into three groups and were fed ad libitum a corn-soya diet balanced in all nutrients. The diet of the experimental quail was supplemented with aurofusarin at the level of 26.4 mg/kg feed in the form of Fusarium graminearum culture enriched with aurofusarin or with aurofusarin plus Mycosorb at 1 g/kg feed. Eggs obtained after 8 weeks of feeding were analysed and incubated in standard conditions of 37.5 degrees C/55% RH. Samples of quail liver were collected from day-old hatchlings. Main polyunsaturated fatty acids (PUFAs) of the egg yolk were analysed by gas chromatography, and tocopherols and tocotrienols were analysed by HPLC-based methods. Inclusion of aurofusarin in the maternal diet was associated with decreased proportions of docosahexaenoic acid and increased proportions of linoleic acid in major lipid fractions of the egg yolk as well as with decreased concentrations of alpha- and gamma-tocopherols, alpha- and gamma-tocotrienols in egg yolk and liver of a day-old quail. Inclusion of modified glucomannans (Mycosorb) into the quail diet simultaneously with aurofusarin showed a significant protective effect against changes in PUFA and antioxidant composition in the egg yolk and liver of quail. It is suggested that a combination of mycotoxin adsorbents and natural antioxidants could be the next step in counteracting mycotoxins in animal feed.
PMID: 12927908 [PubMed - indexed for MEDLINE]

 

Comp Biochem Physiol C Toxicol Pharmacol. 2007 May;145(4):582-7. Epub 2007 Feb 12.

Protective effect of modified glucomannans and organic selenium against antioxidant depletion in the chicken liver due to T-2 toxin-contaminated feed consumption.

Dvorska JE1, Pappas AC, Karadas F, Speake BK, Surai PF.

Abstract
The aim of this work was to assess the effect of T-2 toxin on the antioxidant status of the chicken and to study possible protective effects of modified glucomannan (Mycosorb) and organic selenium (Sel-Plex). Inclusion of T-2 toxin in the chickens' diet (8.1 mg/kg for 21 days) was associated with significant decreases in the concentrations of selenium (Se)(by 32.2%), alpha-tocopherol (by 41.4%), total carotenoids (by 56.5%), ascorbic acid (by 43.5%) and reduced glutathione (by 56.3%) in the liver, as well as a decrease in the hepatic activity of Se-dependent glutathione peroxidase (Se-GSH-Px) (by 36.8%). However, inclusion of modified glucomannans into the T-2 toxin-contaminated diet provided a partial protection against the detrimental effects of the mycotoxin on the antioxidant defences in the chicken liver. For example, the Se concentration in the liver was restored completely, although the Se-GSH-Px activity in the liver increased to only 81% of its control value. These protective effects of modified glucomannas were associated with a 45% reduction of lipid peroxidation in the liver in comparison to the effects of T-2 toxin alone. A combination of modified glucomannas with organic Se was shown to provide further protection against toxin-induced antioxidant depletion and lipid peroxidation in the chicken liver. Thus, the data clearly indicate a major protective effect of the mycotoxin-binder in combination with organic Se against the detrimental consequences of T-2 toxin-contaminated feed consumption by growing chickens.
PMID: 17350343 [PubMed - indexed for MEDLINE]

Trichothecene mycotoxins have a strong immunosuppressive effect. These mycotoxins suppress the host immunity and make them more sensitive to the infection of pathogens, including bacteria and viruses

 

Trichothecene Research

Toxicol Sci.  2008; 104(1):4-26 (ISSN: 1096-0929)

Stachybotrys chartarum, trichothecene mycotoxins, and damp building-related illness: new insights into a public health enigma.

Pestka JJ; Yike I; Dearborn DG; Ward MD; Harkema JR

Abstract

Damp building-related illnesses (DBRI) include a myriad of respiratory, immunologic, and neurologic symptoms that are sometimes etiologically linked to aberrant indoor growth of the toxic black mold, Stachybotrys chartarum. Although supportive evidence for such linkages is limited, there are exciting new findings about this enigmatic organism relative to its environmental dissemination, novel bioactive components, unique cellular targets, and molecular mechanisms of action which provide insight into the S. chartarum's potential to evoke allergic sensitization, inflammation, and cytotoxicity in the upper and lower respiratory tracts. Macrocyclic trichothecene mycotoxins, produced by one chemotype of this fungus, are potent translational inhibitors and stress kinase activators that appear to be a critical underlying cause for a number of adverse effects. Notably, these toxins form covalent protein adducts in vitro and in vivo and, furthermore, cause neurotoxicity and inflammation in the nose and brain of the mouse. A second S. chartarum chemotype has recently been shown to produce atranones-mycotoxins that can induce pulmonary inflammation. Other biologically active products of this fungus that might contribute to pathophysiologic effects include proteinases, hemolysins, beta-glucan, and spirocyclic drimanes. Solving the enigma of whether Stachybotrys inhalation indeed contributes to DBRI will require studies of the pathophysiologic effects of low dose chronic exposure to well-characterized, standardized preparations of S. chartarum spores and mycelial fragments, and, coexposures with other environmental cofactors. Such studies must be linked to improved assessments of human exposure to this fungus and its bioactive constituents in indoor air using both state-of-the-art sampling/analytical methods and relevant biomarkers.

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