T-2 mycotoxin

Last updated
T-2 [1]
T-2 mycotoxin.png
T-2 mycotoxin flat.png
Names
IUPAC name
(2α,3α,4β,8α)-4,15-bis(acetyloxy)-3-hydroxy-12,13-epoxytrichothec-9-en-8-yl 3-methylbutanoate
Other names
T-2 Toxin
Fusariotoxin T 2
Insariotoxin
Mycotoxin T 2
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
ECHA InfoCard 100.040.255 OOjs UI icon edit-ltr-progressive.svg
PubChem CID
RTECS number
  • YD0100000
UNII
  • InChI=1S/C24H34O9/c1-12(2)7-18(27)32-16-9-23(10-29-14(4)25)17(8-13(16)3)33-21-19(28)20(31-15(5)26)22(23,6)24(21)11-30-24/h8,12,16-17,19-21,28H,7,9-11H2,1-6H3/t16-,17+,19+,20+,21+,22+,23+,24-/m0/s1 Yes check.svgY
    Key: BXFOFFBJRFZBQZ-QYWOHJEZSA-N Yes check.svgY
  • InChI=1/C24H34O9/c1-12(2)7-18(27)32-16-9-23(10-29-14(4)25)17(8-13(16)3)33-21-19(28)20(31-15(5)26)22(23,6)24(21)11-30-24/h8,12,16-17,19-21,28H,7,9-11H2,1-6H3/t16-,17+,19+,20+,21+,22+,23+,24-/m0/s1
    Key: BXFOFFBJRFZBQZ-QYWOHJEZBH
  • O=C(O[C@@H]4C(=C/[C@H]3O[C@H]2[C@]1(OC1)[C@]([C@H](OC(=O)C)[C@H]2O)([C@@]3(COC(=O)C)C4)C)\C)CC(C)C
Properties
C24H34O9
Molar mass 466.527 g·mol−1
Insoluble
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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T-2 mycotoxin is a trichothecene mycotoxin. It is a naturally occurring mold byproduct of Fusarium spp. fungus which is toxic to humans and other animals. The clinical condition it causes is alimentary toxic aleukia and a host of symptoms related to organs as diverse as the skin, airway, and stomach. Ingestion may come from consumption of moldy whole grains. T-2 can be absorbed through human skin. [2] Although no significant systemic effects are expected after dermal contact in normal agricultural or residential environments, local skin effects can not be excluded. Hence, skin contact with T-2 should be limited.

Contents

History

Alimentary toxic aleukia (ATA), a disease which is caused by trichothecenes like T-2 mycotoxin, killed many thousands of USSR citizens in the Orenburg District in the 1940s. It was reported that the mortality rate was 10% of the entire population in that area. During the 1970s it was proposed that the consumption of contaminated food was the cause of this mass poisoning. Because of World War II, harvesting of grains was delayed and food was scarce in Russia. This resulted in the consumption of grain that was contaminated with Fusarium molds, which produce T-2 mycotoxin. [3]

In 1981, the United States Secretary of State Alexander Haig and his successor George P. Shultz accused the Soviet Union of using T-2 mycotoxin as a chemical weapon known as "yellow rain" in Laos (1975–81), Kampuchea (1979–81), and Afghanistan (1979–81), where it allegedly caused thousands of casualties. [4] Although several US chemical weapons experts claim to have identified "yellow rain" samples from Laos as trichothecenes, other experts believe that this exposure was due to naturally occurring T-2 mycotoxin in contaminated foods. [5] Another alternative theory was developed by Harvard biologist Matthew Meselson, who proposed that the "yellow rain" found in Southeast Asia originated from the excrement of jungle bees. [6] The first indication for this theory came from finding high levels of pollen in the collected samples, giving the substance its yellow color. It was also found that jungle bees in this area fly collectively in great numbers, at altitudes too high to be easily seen, producing showers of feces that could have been mistaken for sprays from aircraft. [7] Further testing later determined that the oily liquid was, in fact, the pollen-filled feces of jungle bees. [6] A similar case in China was brought to light, and in this instance the cause of the phenomenon had also been bee excrement. [8] Despite this conclusive analysis, the United States has not withdrawn its allegations and declares that the issue has not been fully resolved.

T-2 mycotoxin is also thought to be a cause of Gulf War syndrome. US troops suffered from mycotoxicosis-like symptoms after an Iraqi missile detonated in a US military camp in Saudi Arabia during Operation Desert Storm in the Persian Gulf War, in 1991. It has been shown that Iraq researched trichothecene mycotoxins, among other substances, and thus was capable of its possession and employment in chemical warfare. Nevertheless, much of the key information from these incidents remains classified, leaving these matters still unresolved. [9]

Chemical properties

This compound has a tetracyclic sesquiterpenoid 12,13-epoxytrichothene ring system, which relates it to the trichothecenes. [10] These compounds are generally very stable and are not degraded during storage/milling and cooking/processing of food. They do not degrade at high temperatures either. This compound has an epoxide ring, and several acetyl and hydroxyl groups on its side chains. These features are mainly responsible for the biological activity of the compound and make it highly toxic. T-2 mycotoxin is able to inhibit DNA and RNA synthesis in vivo and in vitro [11] and can induce apoptosis. [12] However, in vivo the compound rapidly metabolizes to HT-2 mycotoxin (a major metabolite). [13]

Mechanism of action

The toxicity of T-2 toxin is due to its 12,13-epoxy ring. [14] Epoxides are in general toxic compounds; these react with nucleophiles and then undergo further enzymatic reactions. The reactivity of epoxides can lead to reactions with endogenous compounds and cellular constituents like DNA bases and proteins. [15] These reactions could be the reason for the noticed actions and effects of T-2 mycotoxin. The toxic compound influences the metabolism of membrane phospholipids, leads to an increase of liver lipid peroxidases and has an inhibiting effect on DNA and RNA synthesis. In addition it can bind to an integral part of the 60s ribosomal subunit, peptidyltransferase, thereby inhibiting protein synthesis. These effects are thought to be the explanation for T-2 toxin inducing apoptosis (cell death) in different tissues as the immune system, the gastrointestinal tissue and also fetal tissue. With regard to apoptosis there has been noticed that the level of the pro-apoptotic factor Bas (Bcl-2-associated X protein) was increased and the level of Bcl-xl, an anti-apoptotic factor, was decreased in human chrondocytes (cartilage cells). When exposed to T-2 mycotoxin. Furthermore, the level of Fas, an apoptosis-related cell-surface antigen and p53, a protein regulating the cell cycle, were increased.

Simplified biosynthesis of the T-2 Mycotoxin in F. sporotrichioides T-2 Mycotoxin Biosynthesis.png
Simplified biosynthesis of the T-2 Mycotoxin in F. sporotrichioides

Synthesis

T-2 mycotoxin is produced naturally by Fusarium fungi of which the most important species are: F. sporotrichioides, F. langsethiae, F. acuminatum and F. poae. These fungi are found in grains such as barley, wheat and oats. The production of this compound for research and commercial purposes is generally accomplished by cultivating some strain of T-2 mycotoxin producing fungi on agar plates. On these agar plates the fungi appear powdery and can yield substantial amounts of T-2 mycotoxin. For the isolation of the compound high pressure liquid chromatography is commonly used (HPLC). [16]

In the Fusarium species, biosynthesis of the T-2 mycotoxin often starts with trichodiene, and many of the species share a common route of oxidizations and cyclizations. As an example, from the F. sporotrichioides species, the important oxidation steps that occur start from trichodiene and goes to isotrichodiol. From there, the eleventh carbon atom is oxidized to form isotrichotriol. The ninth carbon is then oxidized, and trichotriol is formed, which then cyclizes to make isotrichodermol. After that, the fifteenth carbon is oxidized to form didecalonectrin, which leads to the fourth carbon being oxidized, and diacetoxyscirpenol is formed. The second to last step is the oxidation of the eighth carbon to make neosolaniol, which then undergoes slight modification to create the T-2 toxin. [17]

Toxicity

ADME properties

Absorption and exposure

Humans and animals are generally exposed to T-2 mycotoxins through food. Certain grains can contain the toxin which makes it a threat to human health and an economic burden. [18] Unlike most biological toxins T-2 mycotoxin can be absorbed through intact skin. The compound can be delivered via food, water, droplets, aerosols and smoke from various dispersal systems. This makes it a potential biological weapon, however large amounts of the compound are required for a lethal dose. T-2 mycotoxin has an LD50 of approximately 1 milligram per kilogram of body weight.

The EFSA estimates that the mean exposure of T-2 in the EU lies between 12 and 43 ng/kg bw/day. [19] This range is below the TDI of 100 ng/ kg body weight for the sum of HT-2 and T-2 toxins which is used by the EFSA.

Distribution

T-2 mycotoxin is distributed uniformly throughout the body without preference to a specific organ or site. In rodents, plasma concentration levels peak around roughly thirty minutes after exposure, and in one study, the half-life of the T-2 toxin was seen to be less than twenty minutes. In a different study involving pigs, the distribution after four hours of IV injection was seen to be 15–24% in the GI tract and 4.7–5.2% in various other tissues. [20]

Metabolism

Once absorbed and distributed to various tissues, the T-2 mycotoxin goes through various metabolic reactions before it gets excreted. In vivo studies showed that the most occurring reactions are ester hydrolysis and hydroxylation of the isovaleryl group. Deepoxidation and glucuronide conjugation do also occur. Ht-2 is the main metabolite. For the hydroxylation, the cytochrome p450 enzyme complex is suggested to be involved. T-2 triol and T-2 tetraol are most likely to be formed via acetylcholine esterases. Some of the metabolic reactions of the mycotoxin are performed by the microflora in the gut. The formed metabolites in these reactions are species- and pH-dependent. The ester cleavages are however performed by the mammal itself and not by the microflora. In red blood cells T-2 mycotoxin is metabolized to neosolaniol, and, in white blood cells, to HT-2 via hydrolysis catalyzed by carboxylesterases.

Excretion

Following absorption, distribution, and metabolism, T-2 mycotoxin is excreted fairly quickly, where 80–90% of it is excreted within 48 hours. [20] The main methods of excretion seem to be from the urine and feces, [21] where excretion through bile contributes heavily to the feces route of excretion. [14] There is also very little of the parent T-2 mycotoxin in the excretions, meaning most of the initial compound is metabolized beforehand. [21]

Toxic effects

T-2 is highly toxic when inhaled. Acute toxic symptoms include vomiting, diarrhea, skin irritation, itching, rash, blisters, bleeding and dyspnea. [22] If the individual is exposed to T-2 over a longer period alimentary toxic aleukia (ATA) develops.

At first the patient experiences a burning sensation in the mouth, throat and stomach. After a few days the person will suffer from an acute gastroenteritis that will last for 3 to 9 days. Within 9 weeks the bone marrow will slowly degenerate. Also the skin starts bleeding and the total number of leukocytes decreases. Problems with the nervous system can occur.

In the end the following symptoms might occur: a high fever, petechial haemorrhage, necrosis of muscles and skin, bacterial infections of the necrotic tissue, enlarged lymph nodes. There is the possibility of asphyxiation because of laryngeal oedema and stenosis of the glottis. The lack of oxygen is then the cause of death. Otherwise the patient will die of bronchial pneumonia and lung bleeding. [23]

Effects on animals

T-2 mycotoxin is also toxic to animals. The compound is known for having lethal and sub-lethal effects on farm animals. It is often found in contaminated cereal grains that are fed to these animals. [24] Most of the toxic effects are shared between humans and animals. After exposing zebra fish embryos to a concentration of 20 μmol/L or higher malformation and mortality rates increased. The malformations included tail deformities, cardiovascular defects and changes in behavior in early stages of life. This is the result of an increase in the amount of epoxides, which causes cell apoptosis. [25] Other studies have shown that T-2-toxin causes lipid peroxidation in rats after feeding it to them. As the effect of T-2 toxin, elevated reactive oxygen species (ROS) levels were observed in several mammalian species. However, in spite of the general harmful effects caused by the toxin, in a study carried out in different chicken derived hepatic cell culture models, no alterations were found in the redox status of the cells. [26]

The compound also seems to reduce the fertility of ewes and heifers. Research has shown that a high dose of T-2 delays the ovulation due to a delayed follicle maturation. This possibly retards the following luteinisation, which makes it impossible for female animals to conceive.

T-2 also has an effect on the fertility of bulls. In 1998 it was discovered that moldy hay influenced the quality of semen of bulls. Analysis of the moldy hay showed that T-2 was present. The compound decreased sperm motility and testosterone levels and increased the frequency of morphological abnormalities in the sperm cells.

The liver is another target for the mycotoxin. It is one of the first organs where the compound passes through after ingestion. Here it causes a reduced expression of CYP1A proteins in rabbits, pigs and rats. CYP3A activity decreases in pigs too. These enzymes help metabolize drugs that pass through the liver. Decrease in the activity could lead to an increase of unmetabolized drugs in the plasma. This can have a dangerous effect on an animal's health. [27]

All of the mentioned effects happen when T-2 is ingested in high doses. Animals are able to metabolize the compound with enzymes from the CYP3A family, just like humans.

Treatments

At the moment, there is no specific therapy for T-2 mycotoxin poisonings. [21] Exposure of the mycotoxin is typically followed by standardized treatment for toxic compounds in order to reduce the effect of the toxin. This includes using activated charcoal, which has a high binding capacity of 0.48 mg of T-2 mycotoxin to 1 mg of charcoal. [21] For dermal contact, soap and water is used to reduce the dermal effects. [21] As a kind of prophylaxis, antioxidants are believed to have properties that may provide benefits. [20]

Application

There are currently no applications, aside from war, for T-2 mycotoxins; however, there are some plausible therapeutic uses. Due to their abilities, research shows possible uses for the mycotoxin as growth promoters, antibiotics, antivirals, as an antileukemic, and as an antimalarial. [20]

See also

Related Research Articles

<span class="mw-page-title-main">Toxin</span> Naturally occurring organic poison

A toxin is a naturally occurring organic poison produced by metabolic activities of living cells or organisms. They occur especially as proteins, often conjugated. The term was first used by organic chemist Ludwig Brieger (1849–1919) and is derived from the word "toxic".

<span class="mw-page-title-main">Aflatoxin</span> Group of poisons produced by moulds

Aflatoxins are various poisonous carcinogens and mutagens that are produced by certain molds, particularly Aspergillus species mainly by Aspergillus flavus and Aspergillus parasiticus. According to the USDA, "They are probably the best known and most intensively researched mycotoxins in the world." The fungi grow in soil, decaying vegetation and various staple foodstuffs and commodities such as hay, maize, peanuts, coffee, wheat, millet, sorghum, cassava, rice, chili peppers, cottonseed, tree nuts, sesame seeds, sunflower seeds, and various cereal grains and oil seeds. In short, the relevant fungi grow on almost any crop or food. When such contaminated food is processed or consumed, the aflatoxins enter the general food supply. They have been found in both pet and human foods, as well as in feedstocks for agricultural animals. Animals fed contaminated food can pass aflatoxin transformation products into milk, milk products, and meat. For example, contaminated poultry feed is the suspected source of aflatoxin-contaminated chicken meat and eggs in Pakistan.

<span class="mw-page-title-main">Foodborne illness</span> Illness from eating spoiled food

Foodborne illness is any illness resulting from the contamination of food by pathogenic bacteria, viruses, or parasites, as well as prions, and toxins such as aflatoxins in peanuts, poisonous mushrooms, and various species of beans that have not been boiled for at least 10 minutes.

A mycotoxin is a toxic secondary metabolite produced by fungi and is capable of causing disease and death in both humans and other animals. The term 'mycotoxin' is usually reserved for the toxic chemical products produced by fungi that readily colonize crops.

Abraham Z. Joffe (1909–2000) was Professor of Mycology and Mycotoxicology at the Hebrew University, Jerusalem.

<span class="mw-page-title-main">Fumonisin B1</span> Chemical compound

Fumonisin B1 is the most prevalent member of a family of toxins, known as fumonisins, produced by multiple species of Fusarium molds, such as Fusarium verticillioides, which occur mainly in maize (corn), wheat and other cereals. Fumonisin B1 contamination of maize has been reported worldwide at mg/kg levels. Human exposure occurs at levels of micrograms to milligrams per day and is greatest in regions where maize products are the dietary staple.

Yellow rain was a 1981 political incident in which the United States Secretary of State Alexander Haig accused the Soviet Union of supplying T-2 mycotoxin to the communist states in Vietnam, Laos and Cambodia for use in counterinsurgency warfare. Refugees described many different forms of "attacks", including a sticky yellow liquid falling from planes or helicopters, which was dubbed "yellow rain". The U.S. government alleged that over ten thousand people had been killed in attacks using these supposed chemical weapons. The Soviets denied these claims and an initial United Nations investigation was inconclusive.

<span class="mw-page-title-main">Trichothecene</span> Large family of chemically related mycotoxins

The trichothecenes are a large family of chemically related mycotoxins. They are produced by various species of Fusarium, Myrothecium, Trichoderma/Podostroma, Trichothecium, Cephalosporium, Verticimonosporium, and Stachybotrys. Chemically, trichothecenes are a class of sesquiterpenes.

<span class="mw-page-title-main">Zearalenone</span> Chemical compound

Zearalenone (ZEN), also known as RAL and F-2 mycotoxin, is a potent estrogenic metabolite produced by some Fusarium and Gibberella species. Specifically, the Gibberella zeae, the fungal species where zearalenone was initially detected, in its asexual/anamorph stage is known as Fusarium graminearum. Several Fusarium species produce toxic substances of considerable concern to livestock and poultry producers, namely deoxynivalenol, T-2 toxin, HT-2 toxin, diacetoxyscirpenol (DAS) and zearalenone. Particularly, ZEN is produced by Fusarium graminearum, Fusarium culmorum, Fusarium cerealis, Fusarium equiseti, Fusarium verticillioides, and Fusarium incarnatum. Zearalenone is the primary toxin that binds to estrogen receptors, causing infertility, abortion or other breeding problems, especially in swine. Often, ZEN is detected together with deoxynivalenol in contaminated samples and its toxicity needs to be considered in combination with the presence of other toxins.

<span class="mw-page-title-main">Ochratoxin A</span> Chemical compound

Ochratoxin A—a toxin produced by different Aspergillus and Penicillium species — is one of the most-abundant food-contaminating mycotoxins. It is also a frequent contaminant of water-damaged houses and of heating ducts. Human exposure can occur through consumption of contaminated food products, particularly contaminated grain and pork products, as well as coffee, wine grapes, and dried grapes. The toxin has been found in the tissues and organs of animals, including human blood and breast milk. Ochratoxin A, like most toxic substances, has large species- and sex-specific toxicological differences.

<span class="mw-page-title-main">Citrinin</span> Chemical compound

Citrinin is a mycotoxin which is often found in food. It is a secondary metabolite produced by fungi that contaminates long-stored food and it causes different toxic effects, like nephrotoxic, hepatotoxic and cytotoxic effects. Citrinin is mainly found in stored grains, but sometimes also in fruits and other plant products.

<span class="mw-page-title-main">Fumonisin</span> Group of chemical compounds

The fumonisins are a group of mycotoxins derived from Fusarium and their Liseola section. They have strong structural similarity to sphinganine, the backbone precursor of sphingolipids.

Mycotoxicology is the branch of mycology that focuses on analyzing and studying the toxins produced by fungi, known as mycotoxins. In the food industry it is important to adopt measures that keep mycotoxin levels as low as practicable, especially those that are heat-stable. These chemical compounds are the result of secondary metabolism initiated in response to specific developmental or environmental signals. This includes biological stress from the environment, such as lower nutrients or competition for those available. Under this secondary path the fungus produces a wide array of compounds in order to gain some level of advantage, such as incrementing the efficiency of metabolic processes to gain more energy from less food, or attacking other microorganisms and being able to use their remains as a food source.

Fusarium sporotrichioides is a fungal plant pathogen, one of various Fusarium species responsible for damaging crops, in particular causing a condition known as Fusarium head blight in wheat, consequently being of notable agricultural and economic importance. The species is ecologically widespread, being found across tropical and temperate regions, and is a significant producer of mycotoxins, particularly trichothecenes. Although mainly infecting crops, F. sporotrichioides-derived mycotoxins can have repercussions for human health in the case of the ingestion of infected cereals. One such example includes the outbreak of alimentary toxic aleukia (ATA) in Russia, of which F. sporotrichioides-infected crop was suspected to be the cause. Although current studies on F. sporotrichioides are somewhat limited in comparison to other species in the genus, Fusarium sporotrichioides has found several applications as a model system for experimentation in molecular biology.

<span class="mw-page-title-main">Vomitoxin</span> Fungal toxic chemical in grains

Vomitoxin, also known as deoxynivalenol (DON), is a type B trichothecene, an epoxy-sesquiterpenoid. This mycotoxin occurs predominantly in grains such as wheat, barley, oats, rye, and corn, and less often in rice, sorghum, and triticale. The occurrence of deoxynivalenol is associated primarily with Fusarium graminearum and F. culmorum, both of which are important plant pathogens which cause fusarium head blight in wheat and gibberella or fusarium ear blight in corn. The incidence of fusarium head blight is strongly associated with moisture at the time of flowering (anthesis), and the timing of rainfall, rather than the amount, is the most critical factor. However, increased amount of moisture towards harvest time has been associated with lower amount of vomitoxin in wheat grain due to leaching of toxins. Furthermore, deoxynivalenol contents are significantly affected by the susceptibility of cultivars towards Fusarium species, previous crop, tillage practices, and fungicide use. It occurs abundantly in grains in Norway due to heavy rainfall.

Mycoestrogens are xenoestrogens produced by fungi. They are sometimes referred to as mycotoxins. Among important mycoestrogens are zearalenone, zearalenol and zearalanol. Although all of these can be produced by various Fusarium species, zearalenol and zearalanol may also be produced endogenously in ruminants that have ingested zearalenone. Alpha-zearalanol is also produced semisynthetically, for veterinary use; such use is prohibited in the European Union.

Microbial toxins are toxins produced by micro-organisms, including bacteria, fungi, protozoa, dinoflagellates, and viruses. Many microbial toxins promote infection and disease by directly damaging host tissues and by disabling the immune system. Endotoxins most commonly refer to the lipopolysaccharide (LPS) or lipooligosaccharide (LOS) that are in the outer plasma membrane of Gram-negative bacteria. The botulinum toxin, which is primarily produced by Clostridium botulinum and less frequently by other Clostridium species, is the most toxic substance known in the world. However, microbial toxins also have important uses in medical science and research. Currently, new methods of detecting bacterial toxins are being developed to better isolate and understand these toxins. Potential applications of toxin research include combating microbial virulence, the development of novel anticancer drugs and other medicines, and the use of toxins as tools in neurobiology and cellular biology.

Aflatoxin B<sub>1</sub> Chemical compound

Aflatoxin B1 is an aflatoxin produced by Aspergillus flavus and A. parasiticus. It is a very potent carcinogen with a TD50 3.2 μg/kg/day in rats. This carcinogenic potency varies across species with some, such as rats and monkeys, seemingly much more susceptible than others. Aflatoxin B1 is a common contaminant in a variety of foods including peanuts, cottonseed meal, corn, and other grains; as well as animal feeds. Aflatoxin B1 is considered the most toxic aflatoxin and it is highly implicated in hepatocellular carcinoma (HCC) in humans. In animals, aflatoxin B1 has also been shown to be mutagenic, teratogenic, and to cause immunosuppression. Several sampling and analytical methods including thin-layer chromatography (TLC), high-performance liquid chromatography (HPLC), mass spectrometry, and enzyme-linked immunosorbent assay (ELISA), among others, have been used to test for aflatoxin B1 contamination in foods. According to the Food and Agriculture Organization (FAO), a division of the United Nations, the worldwide maximum tolerated levels of aflatoxin B1 was reported to be in the range of 1–20 μg/kg (or .001 ppm - 1 part-per-billion) in food, and 5–50 μg/kg (.005 ppm) in dietary cattle feed in 2003.

<span class="mw-page-title-main">Verrucarin A</span> Chemical compound

Verrucarin A is a chemical compound that belongs in the class of trichothecenes, a group of sesquiterpene toxins produced by several fungi, namely from the Fusarium species, that are responsible for infecting food grains. Within the skeleton of the basic trichothecene structure, the olefin and epoxide are crucial for toxicity; ester functionalities and hydroxyl groups often contribute to the toxicity, thereby rendering verrucarin A as one of the most lethal examples. The mechanism of action for this class of toxins mainly inhibits protein biosynthesis by preventing peptidyl transferase activity. Although initially thought to be potentially useful as anticancer therapeutics, numerous examples of trichothecene derivatives were shown to be too toxic for clinical use.

<span class="mw-page-title-main">Nivalenol</span> Type of mycotoxin

Nivalenol (NIV) is a mycotoxin of the trichothecene group. In nature it is mainly found in fungi of the Fusarium species. The Fusarium species belongs to the most prevalent mycotoxin producing fungi in the temperate regions of the northern hemisphere, therefore making them a considerable risk for the food crop production industry.

References

  1. ↑ "T-2 Toxin: essential data". CBWInfo.com. Archived from the original on October 12, 2008.
  2. ↑ Boonen J, Malysheva SV, Taevernier L, Diana Di Mavungu J, De Saeger S, De Spiegeleer B (November 2012). "Human skin penetration of selected model mycotoxins". Toxicology. 301 (1–3): 21–32. doi:10.1016/j.tox.2012.06.012. PMID   22749975.
  3. ↑ Pitt JI (July 1989). Semple RL, Frio AS, Hicks PA, Lozare JW (eds.). An introduction to mycotoxins. Mycotoxin Prevention and kontrol in Food Grains. Proceedimgs of Assistance for The Training Course. Bangkok.
  4. ↑ Shultz GP (1982). Chemical warfare in Southeast Asia and Afghanistan: an update (Report). US Department of State, Bureau of Public Affairs, Office of Public Communication, Editorial Division.
  5. ↑ Caldwell RD (1983). "'Yellow rain' or natural toxins?". Nature. 301 (5902): 651. Bibcode:1983Natur.301Q.651C. doi: 10.1038/301651a0 . S2CID   4263047.
  6. 1 2 "Yellow Rain Falls". New York Times. September 3, 1987. Archived from the original on November 9, 2012. Retrieved January 20, 2022. Yellow rain is the excrement of jungle bees. It's yellow from digested pollen grains, and it rains down from swarms of bees too high to be seen. His theory turns out to be exactly right. The Government's own studies, still unpublished, prove that the source is bees, not bombs.
  7. ↑ Meselson MS, Robinson JP (June 2008). "The Yellow Rain Affair: Lessons from a Discredited Allegation". In Clunan AL, Lavoy PR, Martin SB (eds.). Terrorism, War, or Disease? Unraveling the Use of Biological Weapons. Stanford: Stanford University Press. pp. 72–96. Archived from the original on 2014-07-27. Retrieved 2015-09-03.
  8. ↑ Zhang Z (1977). "A Study of the Origin and the Pollen Analysis of "Yellow Rain" in Northern Jiangsu". Kexue Tongbao. 22: 409–12.
  9. ↑ Zilinskas RA (August 1997). "Iraq's biological weapons. The past as future?". JAMA. 278 (5): 418–424. doi:10.1001/jama.1997.03550050080037. PMID   9244334.
  10. ↑ CBRNE - T-2 Mycotoxins at eMedicine
  11. ↑ Marin S, Ramos AJ, Cano-Sancho G, Sanchis V (October 2013). "Mycotoxins: occurrence, toxicology, and exposure assessment". Food and Chemical Toxicology. 60: 218–237. doi:10.1016/j.fct.2013.07.047. PMID   23907020.
  12. ↑ Torp M, Langseth W (1999). "Production of T-2 toxin by a Fusarium resembling Fusarium poae". Mycopathologia. 147 (2): 89–96. doi:10.1023/A:1007060108935. PMID   10967967. S2CID   13540977.
  13. ↑ Wu QH, Wang X, Yang W, Nüssler AK, Xiong LY, Kuča K, et al. (July 2014). "Oxidative stress-mediated cytotoxicity and metabolism of T-2 toxin and deoxynivalenol in animals and humans: an update". Archives of Toxicology. 88 (7): 1309–1326. doi:10.1007/s00204-014-1280-0. PMID   24894432. S2CID   14146122.
  14. 1 2 Li Y, Wang Z, Beier RC, Shen J, De Smet D, De Saeger S, Zhang S (April 2011). "T-2 toxin, a trichothecene mycotoxin: review of toxicity, metabolism, and analytical methods". Journal of Agricultural and Food Chemistry. 59 (8): 3441–3453. doi:10.1021/jf200767q. PMID   21417259.
  15. ↑ Timbrell JA (2013-01-28). Principles of Biochemical Toxicology (4th ed.). Boca Raton: CRC Press. doi:10.3109/9781420007084. ISBN   978-0-429-12493-8.
  16. ↑ "T-2 toxin from fusarium sp., powder, ≥98% (HPLC)". Sigma-Aldridge.
  17. ↑ Desjardins AE, Hohn TM, McCormick SP (September 1993). "Trichothecene biosynthesis in Fusarium species: chemistry, genetics, and significance". Microbiological Reviews. 57 (3): 595–604. doi:10.1128/MMBR.57.3.595-604.1993. PMC   372927 . PMID   8246841.
  18. ↑ Wan Q, Wu G, He Q, Tang H, Wang Y (March 2015). "The toxicity of acute exposure to T-2 toxin evaluated by the metabonomics technique". Molecular BioSystems. 11 (3): 882–891. doi:10.1039/C4MB00622D. PMID   25588579.
  19. ↑ Escrivá L, Font G, Manyes L (April 2015). "In vivo toxicity studies of fusarium mycotoxins in the last decade: a review". Food and Chemical Toxicology. 78: 185–206. doi:10.1016/j.fct.2015.02.005. PMID   25680507.
  20. 1 2 3 4 Adhikari M, Negi B, Kaushik N, Adhikari A, Al-Khedhairy AA, Kaushik NK, Choi EH (May 2017). "T-2 mycotoxin: toxicological effects and decontamination strategies". Oncotarget. 8 (20): 33933–33952. doi:10.18632/oncotarget.15422. PMC   5464924 . PMID   28430618.
  21. 1 2 3 4 5 Wannemacher RW, Weiner SL (1997). "Chapter 34: Trichothecene Mycotoxins". Medical aspects of chemical and biological warfare. U.S. Government Printing Office. pp. 655–676. ISBN   9789997320919.
  22. ↑ Kalantari H, Mousavi M (2010). "Review on T-2 Toxin". Jundishapur Journal of Natural Pharmaceutical Products. 5 (1): 26–38.
  23. ↑ Semple RL, Frio AS, Hicks PA, Lozare JV (1989). Mycotoxin prevention and control in foodgrains. UNDP/FAO Regional Network Inter-Country Cooperation on Preharvest Technology and Quality Control of Foodgrains (REGNET) and the ASEAN Grain Postharvest Programme (Report). Thailand.
  24. ↑ Cortinovis C, Pizzo F, Spicer LJ, Caloni F (October 2013). "Fusarium mycotoxins: effects on reproductive function in domestic animals--a review". Theriogenology. 80 (6): 557–564. doi:10.1016/j.theriogenology.2013.06.018. PMID   23916251.
  25. ↑ Yuan G, Wang Y, Yuan X, Zhang T, Zhao J, Huang L, Peng S (April 2014). "T-2 toxin induces developmental toxicity and apoptosis in zebrafish embryos". Journal of Environmental Sciences. 26 (4): 917–925. doi:10.1016/S1001-0742(13)60510-0. PMID   25079423.
  26. ↑ Mackei M, Orbán K, Molnár A, Pál L, Dublecz K, Husvéth F, et al. (January 2020). "Cellular Effects of T-2 Toxin on Primary Hepatic Cell Culture Models of Chickens". Toxins. 12 (1): 46. doi: 10.3390/toxins12010046 . PMC   7020465 . PMID   31941063.
  27. ↑ Goossens J, De Bock L, Osselaere A, Verbrugghe E, Devreese M, Boussery K, et al. (July 2013). "The mycotoxin T-2 inhibits hepatic cytochrome P4503A activity in pigs". Food and Chemical Toxicology. 57: 54–56. doi:10.1016/j.fct.2013.03.009. PMID   23524315.

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