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Academic literature on the topic 'Trichothecene'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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Journal articles on the topic "Trichothecene"

1

Boddu, Jayanand, Seungho Cho, and Gary J. Muehlbauer. "Transcriptome Analysis of Trichothecene-Induced Gene Expression in Barley." Molecular Plant-Microbe Interactions® 20, no. 11 (November 2007): 1364–75. http://dx.doi.org/10.1094/mpmi-20-11-1364.

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Fusarium head blight, caused primarily by Fusarium graminearum, is a major disease problem on barley (Hordeum vulgare L.). Trichothecene mycotoxins produced by the fungus during infection increase the aggressiveness of the fungus and promote infection in wheat (Triticum aestivum L.). Loss-of-function mutations in the TRI5 gene in F. graminearum result in the inability to synthesize trichothecenes and in reduced virulence on wheat. We examined the impact of pathogen-derived trichothecenes on virulence and the transcriptional differences in barley spikes infected with a trichothecene-producing wild-type strain and a loss-of-function tri5 trichothecene nonproducing mutant. Disease severity, fungal biomass, and floret necrosis and bleaching were reduced in spikes inoculated with the tri5 mutant strain compared with the wild-type strain, indicating that the inability to synthesize trichothecenes results in reduced virulence in barley. We detected 63 transcripts that were induced during trichothecene accumulation, including genes encoding putative trichothecene detoxification and transport proteins, ubiquitination-related proteins, programmed cell death-related proteins, transcription factors, and cytochrome P450s. We also detected 414 gene transcripts that were designated as basal defense response genes largely independent of trichothecene accumulation. Our results show that barley exhibits a specific response to trichothecene accumulation that can be separated from the basal defense response. We propose that barley responds to trichothecene accumulation by inducing at least two general responses. One response is the induction of genes encoding trichothecene detoxification and transport activities that may reduce the impact of trichothecenes. The other response is to induce genes encoding proteins associated with ubiquitination and cell death which may promote successful establishment of the disease.

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Nishiuchi, Takumi, Daisuke Masuda, Hideo Nakashita, Kazuya Ichimura, Kazuo Shinozaki, Shigeo Yoshida, Makoto Kimura, Isamu Yamaguchi, and Kazuo Yamaguchi. "Fusarium Phytotoxin Trichothecenes Have an Elicitor-Like Activity in Arabidopsis thaliana, but the Activity Differed Significantly Among Their Molecular Species." Molecular Plant-Microbe Interactions® 19, no. 5 (May 2006): 512–20. http://dx.doi.org/10.1094/mpmi-19-0512.

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Phytopathogenic fungi such as Fusarium spp. synthesize trichothecene family phytotoxins. Although the type B trichothecene, deoxynivalenol (DON), is thought to be a virulence factor allowing infection of plants by their trichothecene-producing Fusarium spp., little is known about effects of trichothecenes on the defense response in host plants. Therefore, in this article, we investigated these effects of various trichothecenes in Fusarium-susceptible Arabidopsis thaliana. Necrotic lesions were observed in Arabidopsis leaves infiltrated by 1 μM type A trichothecenes such as T-2 toxin. Trichothecene-induced lesions exhibited dead cells, callose deposition, generation of hydrogen peroxide, and accumulation of salicylic acids. Moreover, infiltration by trichothecenes caused rapid and prolonged activation of two mitogen-activated protein kinases and induced expression of both PR-1 and PDF1.2 genes. Thus, type A trichothecenes trigger the cell death by activation of an elicitor-like signaling pathway in Arabidopsis. Although DON did not have such an activity even at 10 μM, translational inhibition by DON was observed at concentrations above 5 μM. These results suggested that DON is capable of inhibiting translation in Arabidopsis cells without induction of the elicitor-like signaling pathway.

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3

Polak-Śliwińska, Magdalena, and Beata Paszczyk. "Trichothecenes in Food and Feed, Relevance to Human and Animal Health and Methods of Detection: A Systematic Review." Molecules 26, no. 2 (January 16, 2021): 454. http://dx.doi.org/10.3390/molecules26020454.

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Trichothecene mycotoxins are sesquiterpenoid compounds primarily produced by fungi in taxonomical genera such as Fusarium, Myrothecium, Stachybotrys, Trichothecium, and others, under specific climatic conditions on a worldwide basis. Fusarium mold is a major plant pathogen and produces a number of trichothecene mycotoxins including deoxynivalenol (or vomitoxin), nivalenol, diacetoxyscirpenol, and T-2 toxin, HT-2 toxin. Monogastrics are sensitive to vomitoxin, while poultry and ruminants appear to be less sensitive to some trichothecenes through microbial metabolism of trichothecenes in the gastrointestinal tract. Trichothecene mycotoxins occur worldwide however both total concentrations and the particular mix of toxins present vary with environmental conditions. Proper agricultural practices such as avoiding late harvests, removing overwintered stubble from fields, and avoiding a corn/wheat rotation that favors Fusarium growth in residue can reduce trichothecene contamination of grains. Due to the vague nature of toxic effects attributed to low concentrations of trichothecenes, a solid link between low level exposure and a specific trichothecene is difficult to establish. Multiple factors, such as nutrition, management, and environmental conditions impact animal health and need to be evaluated with the knowledge of the mycotoxin and concentrations known to cause adverse health effects. Future research evaluating the impact of low-level exposure on livestock may clarify the potential impact on immunity. Trichothecenes are rapidly excreted from animals, and residues in edible tissues, milk, or eggs are likely negligible. In chronic exposures to trichothecenes, once the contaminated feed is removed and exposure stopped, animals generally have an excellent prognosis for recovery. This review shows the occurrence of trichothecenes in food and feed in 2011–2020 and their toxic effects and provides a summary of the discussions on the potential public health concerns specifically related to trichothecenes residues in foods associated with the exposure of farm animals to mycotoxin-contaminated feeds and impact to human health. Moreover, the article discusses the methods of their detection.

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4

Foroud, Nora A., Danica Baines, Tatiana Y. Gagkaeva, Nehal Thakor, Ana Badea, Barbara Steiner, Maria Bürstmayr, and Hermann Bürstmayr. "Trichothecenes in Cereal Grains – An Update." Toxins 11, no. 11 (October 31, 2019): 634. http://dx.doi.org/10.3390/toxins11110634.

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Trichothecenes are sesquiterpenoid mycotoxins produced by fungi from the order Hypocreales, including members of the Fusarium genus that infect cereal grain crops. Different trichothecene-producing Fusarium species and strains have different trichothecene chemotypes belonging to the Type A and B class. These fungi cause a disease of small grain cereals, called Fusarium head blight, and their toxins contaminate host tissues. As potent inhibitors of eukaryotic protein synthesis, trichothecenes pose a health risk to human and animal consumers of infected cereal grains. In 2009, Foroud and Eudes published a review of trichothecenes in cereal grains for human consumption. As an update to this review, the work herein provides a comprehensive and multi-disciplinary review of the Fusarium trichothecenes covering topics in chemistry and biochemistry, pathogen biology, trichothecene toxicity, molecular mechanisms of resistance or detoxification, genetics of resistance and breeding strategies to reduce their contamination of wheat and barley.

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Bycroft, Barrie W., Nigel C. P. Baldwin, Paul M. Dewick, David C. Marsh, and John Gilbert. "Trichothecene Mycotoxins from Fusarium culmorum Cultures." Zeitschrift für Naturforschung C 42, no. 9-10 (October 1, 1987): 1043–49. http://dx.doi.org/10.1515/znc-1987-9-1007.

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Chemical analysis of the culture filtrates of Fusarium culmorum CMI 14764 has demonstrated the presence of seven trichothecene mycotoxins. Major metabolites are 3-acetyldeoxynivalenol and 7α,8α-dihydroxycalonectrin. with 3,15-diacetyldeoxynivalenol, deoxynivalenol. calonectrin, isotrichodermin and 12,13-epoxytrichothec-9-ene (EPT) as minor products. The occurrence of the rarely encountered unsubstituted trichothecene EPT is significant in that this compound may function as a common intermediate in the biosynthetic pathways to all natural trichothecenes. The structures of the known trichothecenes isolated from F. culmorum suggest a route in which EPT is sequentially oxygenated to the more complex deoxynivalenol derivatives.

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Meek, Isaac B., Andrew W. Peplow, Charles Ake,, T. D. Phillips, and Marian N. Beremand. "Tri1 Encodes the Cytochrome P450 Monooxygenase for C-8 Hydroxylation during Trichothecene Biosynthesis in Fusarium sporotrichioides and Resides Upstream of Another New Tri Gene." Applied and Environmental Microbiology 69, no. 3 (March 2003): 1607–13. http://dx.doi.org/10.1128/aem.69.3.1607-1613.2003.

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ABSTRACT Many Fusarium species produce one or more agriculturally important trichothecene mycotoxins, and the relative level of toxicity of these compounds is determined by the pattern of oxygenations and acetylations or esterifications on the core trichothecene structure. Previous studies with UV-induced Fusarium sporotrichioides NRRL 3299 trichothecene mutants defined the Tri1 gene and demonstrated that it was required for addition of the oxygen at the C-8 position during trichothecene biosynthesis. We have cloned and characterized the Tri1 gene from NRRL 3299 and found that it encodes a cytochrome P450 monooxygenase. The disruption of Tri1 blocks production of C-8-oxygenated trichothecenes and leads to the accumulation of 4,15-diacetoxyscirpenol, the same phenotype observed in the tri1 UV-induced mutants MB1716 and MB1370. The Tri1 disruptants and the tri1 UV-induced mutants do not complement one another when coinoculated, and the Tri1 gene sequence restores T-2 toxin production in both MB1716 and MB1370. The DNA sequence flanking Tri1 contains another new Tri gene. Thus, Tri1 encodes a C-8 hydroxylase and is located either in a new distal portion of the trichothecene gene cluster or in a second separate trichothecene gene cluster.

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SNYDER, A. PETER. "Qualitative, Quantitative and Technological Aspects of the Trichothecene Mycotoxins." Journal of Food Protection 49, no. 7 (July 1, 1986): 544–69. http://dx.doi.org/10.4315/0362-028x-49.7.544.

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Trichothecene mycotoxins pose a natural threat to plants, foodstuffs, animals and humans. Recently, strong implications regarding artificially induced trichothecene threats to humans in various parts of the world have come to the attention of the general public. This has spawned renewed interest and scientific research into the various properties of the toxins. The trichothecenes display orders of magnitude differences in toxicity levels depending upon the test subject and mode of administration. Potentially more sensitive and specific analytical characterization techniques and convenient, milder and faster organic decontamination reaction schemes exist in comparison to established methods. This review attempts to supply a concise information source as an aid to investigators faced with problems of trichothecene detection, analysis, and decontamination.

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Engler, Kathryn H., Raymond D. Coker, and Ivor H. Evans. "A Colorimetric Technique for Detecting Trichothecenes and Assessing Relative Potencies." Applied and Environmental Microbiology 65, no. 5 (May 1, 1999): 1854–57. http://dx.doi.org/10.1128/aem.65.5.1854-1857.1999.

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ABSTRACT We tested a novel colorimetric toxicity test, based on inhibition of β-galactosidase activity in the yeastKluyveromyces marxianus, for sensitivity to a range of mycotoxins. A variety of trichothecene mycotoxins could be detected. The order of toxicity established with this bioassay was verrucarin A > roridin A > T-2 toxin > diacetoxyscirpenol > HT-2 toxin > acetyl T-2 toxin > neosolaniol > fusarenon X > T-2 triol > scirpentriol > nivalenol > deoxynivalenol > T-2 tetraol. The sensitivity of detection was high, with the most potent trichothecene tested, verrucarin A, having a 50% effective concentration (concentration of toxin causing 50% inhibition) of 2 ng/ml. Other mycotoxins (cyclopiazonic acid, fumonisin B1, ochratoxin A, patulin, sterigmatocystin, tenuazonic acid, and zearalenone) could not be detected at up to 10 μg/ml, nor could aflatoxins B1 and M1 be detected at concentrations up to 25 μg/ml. This test should be useful for trichothecene detection and for studies of relevant interactions—both between trichothecenes themselves and between trichothecenes and other food constituents.

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Zhu, Muzi, Youfei Cen, Wei Ye, Saini Li, and Weimin Zhang. "Recent Advances on Macrocyclic Trichothecenes, Their Bioactivities and Biosynthetic Pathway." Toxins 12, no. 6 (June 23, 2020): 417. http://dx.doi.org/10.3390/toxins12060417.

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Macrocyclic trichothecenes are an important group of trichothecenes bearing a large ring. Despite the fact that many of trichothecenes are of concern in agriculture, food contamination, health care and building protection, the macrocyclic ones are becoming the research hotspot because of their diversity in structure and biologic activity. Several researchers have declared that macrocyclic trichothecenes have great potential to be developed as antitumor agents, due to the plenty of their compounds and bioactivities. In this review we summarize the newly discovered macrocyclic trichothecenes and their bioactivities over the last decade, as well as identifications of genes tri17 and tri18 involved in the trichothecene biosynthesis and putative biosynthetic pathway. According to the search results in database and phylogenetic trees generated in the review, the species of the genera Podostroma and Monosporascus would probably be great sources for producing macrocyclic trichothecenes. Moreover, we propose that the macrocyclic trichothecene roridin E could be formed via acylation or esterification of the long side chain linked with C-4 to the hydroxyl group at C-15, and vice versa. More assays and evidences are needed to support this hypothesis, which would promote the verification of the proposed pathway.

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Tanaka, Nozomu, Ryo Takushima, Akira Tanaka, Ayaki Okada, Kosuke Matsui, Kazuyuki Maeda, Shunichi Aikawa, Makoto Kimura, and Naoko Takahashi-Ando. "Reduced Toxicity of Trichothecenes, Isotrichodermol, and Deoxynivalenol, by Transgenic Expression of the Tri101 3-O-Acetyltransferase Gene in Cultured Mammalian FM3A Cells." Toxins 11, no. 11 (November 10, 2019): 654. http://dx.doi.org/10.3390/toxins11110654.

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In trichothecene-producing fusaria, isotrichodermol (ITDol) is the first intermediate with a trichothecene skeleton. In the biosynthetic pathway of trichothecene, a 3-O-acetyltransferase, encoded by Tri101, acetylates ITDol to a less-toxic intermediate, isotrichodermin (ITD). Although trichothecene resistance has been conferred to microbes and plants transformed with Tri101, there are no reports of resistance in cultured mammalian cells. In this study, we found that a 3-O-acetyl group of trichothecenes is liable to hydrolysis by esterases in fetal bovine serum and FM3A cells. We transfected the cells with Tri101 under the control of the MMTV-LTR promoter and obtained a cell line G3 with the highest level of C-3 acetylase activity. While the wild-type FM3A cells hardly grew in the medium containing 0.40 μM ITDol, many G3 cells survived at this concentration. The IC50 values of ITDol and ITD in G3 cells were 1.0 and 9.6 μM, respectively, which were higher than the values of 0.23 and 3.0 μM in the wild-type FM3A cells. A similar, but more modest, tendency was observed in deoxynivalenol and 3-acetyldeoxynivalenol. Our findings indicate that the expression of Tri101 conferred trichothecene resistance in cultured mammalian cells.

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Dissertations / Theses on the topic "Trichothecene"

1

Widestrand, Johan. "Assessment of trichothecene contamination : chemical aspects and biological methodology /." Uppsala : Swedish Univ. of Agricultural Sciences (Sveriges lantbruksuniv.), 2001. http://epsilon.slu.se/avh/2001/91-576-5808-0.pdf.

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Marsh, David C. "Chemical and biochemical transformations of trichothecene mycotoxins." Thesis, University of Nottingham, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235967.

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Asam, Stefan. "Analytik von Trichothecen-Mykotoxinen." Garching DFA, 2009. http://d-nb.info/994911408/04.

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4

Lévy, Philippe. "La vomitoxine." Strasbourg 1, 1990. http://www.theses.fr/1990STR15014.

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Hesketh, Andrew R. "Metabolic studies on the transformation of trichodiene to trichothecene mycotoxins." Thesis, University of Nottingham, 1991. http://eprints.nottingham.ac.uk/12521/.

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Trichodiene and [14C]trichodiene have been produced in high yields by treatment of Fusarium culmorum CMI 14764 cultures with the furanocoumarin xanthotoxin. Smaller amounts of isotrichodermin (ITD) and the unsubstituted trichothecene 12,13-epoxytrichothec-9-ene (EPT) were obtained in the same way. EPT was also produced by semi-synthesis from ITD. Trichodiene (TDN) was shown to be a precursor of the trichothecene mycotoxins in F. culmorum, including EPT, ITD, calonectrin (CAL), 7a-hydroxycalonectrin (7-hydroxyCAL), 15-deacetylcalonectrin, 3-acetyldeoxynivalenol (3-AcDON) and 7,8-dihydroxycalonectrin (DHC). When large amounts of TDN were supplied, a new trichodiene metabolite was found to accumulate which was fully characterised as 12,13-epoxy-2a, 11 adihydroxytrichodiene, and given the trivial name isotrichodiol. A method for the production of 14C-labelled isotrichodiol (ITdiol) was developed, and the incorporation of ["C]ITdiol into 3-AcDON, DHC and 7-hydroxyCAL was demonstrated. Slow, acid-catalysed cyclisation of ITdiol to EPT and pre-sambucoin was demonstrated, and allylic isomerisation to both 9a- and 9p-trichodiol was also detected. Labelled pre-sambucoin was incorporated into sambucoin by F. culmorwn, and ITdiol is thus proposed as a precursor to both sambucoin and sambucinol, aswel as to the trichothecenes. A range of semi-synthetic derivatives of TDN were prepared and tested as possible inhibitors of the post-TDN biosynthesic pathway to trichothecenes in F. culmorum. In whole-cell systems all the derivatives inhibited the incorporation of labelled TDN into trichothecenes, and also initiated the production of ITdiol. One derivative, 9P, 10ß-epoxytrichodiene, was shown to be biotransformed by the fungus, undergoing 12,13-epoxidation with subsequent hydroxylation at C-3 producing 3a-hydroxy-9(3,10(3; 12,13-diepoxytrichodiene. 9ß-Trichodiol was isolated from Trichothecium roseum, and its slow, acidcatalysed cyclisation to EPT was demonstrated. 9a-Trichotriol, 9ß-trichotriol and isotrichotriol were isolated from F. culmorum for the first time, and literature assignments for the stereochemistry of the C-9 hydroxyl in trichodiol and trichotriol are reassessed. The incorporation of [`4C]ITdiol into trichothecenes in F. culmorum was found to be approximately 5 times greater than the incorporation of [14C]-913-trichotriol, and was shown to be inhibited by isotrichotriol but not by 9ß-trichodiol and 9ß-trichotriol. It is proposed that trichodiol and trichotriol are not biosynthetic intermediates in the pathway to the trichothecenes, and that they are non-enzymic metabolites produced from ITdiol and isotrichotriol, respectively, by acid-catalysed isomerisations. A new scheme for the biosynthesis of trichothecenes is proposed in which ITdiol and isotrichotriol are intermediates in the production of isotrichodermol from TDN. Two novel compounds, 15-deacetyl-7,8-dihydroxycalonectrin (15-deacetylDHC) and 8a-hydroxyisotrichodiol were isolated from F. culmorum, and 15-deacetylDHC and DHC were shown to be precursors to 3-AcDON. It is proposed that the post-cyclisation biosynthesis of 3-AcDON involves sequential oxygenation of isotrichodermol at C-15, C-7 and C-8 producing DHC, which then undergoes deacylation to 15-deacetylDHC followed by oxidation at C-8 to 3-AcDON.

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Ward, Caroline L. "Chemical and biochemical studies on the biosynthesis of trichothecene mycotoxins." Thesis, University of Nottingham, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263003.

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Kim, Yongcheol. "Ribosomal protein gene expression and trichothecene resistance in Arabidopsis thaliana /." The Ohio State University, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487687115927105.

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Janse, Van Rensburg Daniel Francois. "The biological properties of three trichothecene mycotoxins produces by fusaris." Master's thesis, University of Cape Town, 1986. http://hdl.handle.net/11427/27209.

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The highly toxic fungal metabolite, neosolaniol monoacetate, was isolated and purified from cultures of Fusarium sambucinum. Since little is known about its toxic properties, the biological effects of this trichothecene were compared to those caused by diacetoxy-scirpenol in male Wistar rats. The lesions caused by the two toxins were very similar. Chronic exposure to either toxin led to a significant decrease (P<0.05) in red blood cell counts and a significant increase (P<0.05) in platelet size. The major pathological lesions observed were atrophy of the actively dividing cells of the bone marrow, thymus, spleen and lymph nodes. The reported species difference in T-2 toxin toxicity was investigated by determining the deacylation rate of T-2 toxin to HT-2 toxin, one of the first steps in the detoxification of this trichothecene. The high deacylation rate catalysed by rat microsomes correlated with the low sensitivity of this species to T-2 toxin, whereas the low deacylation rates with cat and monkey microsomes agreed with their high sensitivity. In contrast to this, the apparently high toxicity of T-2 toxin to humans does not correlate with the high deacylation rate observed in human hepatic microsomes. Involvement of the UDP-glucuronyltransferases in the detoxification of T-2 toxin was studied with rat and pig hepatic microsomes. T-2 toxin and two of its metabolites, HT-2 toxin and T-2 tetraol, did not appear to act as substrates for these enzymes under the in vitro conditions used.

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Tag, Andrew George. "Characterization of the Tri10 gene from Fusarium sporotrichioides." [College Station, Tex. : Texas A&M University, 2003. http://hdl.handle.net/1969.1/64.

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Thesis (Ph.D.)--Texas A&M University, 2003.
"Major Subject: Plant Pathology" Title from author supplied metadata (record created on Jul. 18, 2005.) Vita. Abstract. Includes bibliographical references.

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Schnerr, Helge. "Quantitativer Nachweis von Deoxynivalenol und Trichothecene-bildenden Fusarium spp. mit Biosensor und PCR in Getreide." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=965200639.

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Books on the topic "Trichothecene"

1

John, Lacey, and International Society for Plant Pathology. Mycotoxicology Committee., eds. Trichothecenes and other mycotoxins: Proceedings of the International Mycotoxin Symposium held in Sydney, Australia, August, 1984. Chichester [West Sussex]: Wiley, 1985.

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The characterization and analysis of trichothecenes by chemical ionization and tandem mass spectrometry. Helsinki: Suomalainen Tiedeakatemia, 1989.

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Additives, Joint FAO/WHO Expert Committee on Food. Evaluation of certain mycotoxins in food: Fifty-sixth report of the joint FAO/WHO Expert Committee on Food Attitives. Geneva: World Health Organization, 2002.

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Joint FAO/WHO Expert Committee on Food Additives. Safety evaluation of certain mycotoxins in food. Geneva: World Health Organization, 2001.

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Moss, Maurice O. Trichothecene Mycotoxins. Cambridge University Press, 2004.

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Richard, Beasley Val, ed. Trichothecene mycotoxicosis: Pathophysiologic effects. Boca Raton, Fla: CRC Press, 1989.

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Beasely, Val Richard. Trichothecene Mycotoxicosis: Pathophysiologic Effects. CRC Press, 1989.

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Trichothecene Mycotoxicosis Pathophysiologic Effects (1989). CRC Press, 2017. http://dx.doi.org/10.1201/9781315121260.

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Trichothecene Mycotoxicosis Pathophysiologic Effects (1989). CRC Press, 2017. http://dx.doi.org/10.1201/9781315121284.

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Beasley, Val Ed. Trichothecene Mycotoxicosis Volume 2: Pathophysiologic Effects. CRC Press, 1989.

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Book chapters on the topic "Trichothecene"

1

Atta-ur-Rahman and Viqar Uddin Ahmad. "Trichothecene." In 13C-NMR of Natural Products, 564–82. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3290-3_36.

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Wei, Songhong, Theo van der Lee, Els Verstappen, Marga van Gent, and Cees Waalwijk. "Targeting Trichothecene Biosynthetic Genes." In Methods in Molecular Biology, 173–89. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6707-0_11.

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Taylor, Michael J. "Immunotoxicity of Trichothecene Mycotoxins." In Biodeterioration Research, 85–101. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4757-9453-3_6.

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Pascale, Michelangelo, Vincenzo Lippolis, Chris M. Maragos, and Angelo Visconti. "Recent Developments in Trichothecene Analysis." In ACS Symposium Series, 192–210. Washington, DC: American Chemical Society, 2008. http://dx.doi.org/10.1021/bk-2008-1001.ch010.

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Stahr, Henry M., Gary D. Osweiler, Paula Martin, Marlaine Domoto, and Brad Debey. "Thermal Detoxification of Trichothecene Contaminated Commodities." In Biodeterioration Research 1, 231–38. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0949-9_24.

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Bata, A., W. V. Dashek, G. C. Llewellyn, T. F. Cheatle, C. E. O’Rear, and B. Harrach. "Quantifying Naturally-Occurrrng Macrocyclic Trichothecene Toxins." In Biodeterioration Research, 253–59. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4757-9453-3_20.

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Kurtz, Harold J. "Comparative pathologic changes in trichothecene toxicosis." In Diagnosis of Mycotoxicoses, 191–94. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4235-6_17.

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McCormick, Susan P., Nancy J. Alexander, and Robert H. Proctor. "Trichothecene Triangle: Toxins, Genes, and Plant Disease." In Phytochemicals, Plant Growth, and the Environment, 1–17. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4066-6_1.

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Sato, Shizuo. "Comparative biochemical changes associated with the trichothecene toxicoses." In Diagnosis of Mycotoxicoses, 113–23. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4235-6_11.

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Swanson, S. P., C. Helaszek, and H. D. Rood. "Biotransformation of Trichothecenes: The Role of Intestinal Microflora in the Metabolism and Toxicity of Trichothecene Mycotoxins." In Microbial Toxins in Foods and Feeds, 467–81. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0663-4_43.

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Conference papers on the topic "Trichothecene"

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Taylor, Laurie. "Use of the volatile trichodiene to reduce Fusarium head blight and trichothecene contamination in wheat." In ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1051756.

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Brasel, T., J. Martin, M. Larranaga, S. Wilson, and D. Straus. "143. Rapid Detection of Airborne Macrocyclic Trichothecene Mycotoxins Produced by Stachybotrys chartarum in the Indoor Environment Using High Volume Liquid Impaction." In AIHce 2004. AIHA, 2004. http://dx.doi.org/10.3320/1.2758114.

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Mateo, E. M., F. M. Valle-Algarra, F. Mateo, M. A. Esparza, and M. Jiménez. "Predictive study of climate change impact on type B trichothecene production by isolates of Fusarium graminearum and F. culmorum infecting wheat in Spain." In MICROBES IN APPLIED RESEARCH - Current Advances and Challenges. WORLD SCIENTIFIC, 2012. http://dx.doi.org/10.1142/9789814405041_0058.

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Reports on the topic "Trichothecene"

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Cook, C. E., M. C. Wani, and C. C. Whisnant. Development of General Antisera for Trichothecanes. Fort Belvoir, VA: Defense Technical Information Center, July 1986. http://dx.doi.org/10.21236/ada178266.

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