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Acetyl-T-2-toxin

Kotsonis FN, Ellison RA, Smalley EB (1975) Isolation of Acetyl-T-2 Toxin from Fusarium poae. Appl Microbiol 30 493... [Pg.120]

Methods exist for many matrix/mycotoxin combinations including patulin in apple juice using atmospheric pressure photoionization, zearalenone and its metabolites in fish tissue and porcine urine, muscle, and liver tissues using electrospray ionization, trichothecenes (T-2 toxin, HT-2 toxin, acetyl T-2 toxin, diacetoxyscirpenol, neosolaniol, and mono-acetoxyscirpenol) in grain using atmospheric pressure chemical ionization, and trichothecenes (T-2 toxin, HT-2 toxin, deoxynivalenol, nivalenol), zearalenone and its metabolites (a- and jS-zearalenol and a- and jS-zearalanol) in eggs. [Pg.1513]

FsTril6 (encoding an acyltransferase necessary for formation of ester side chain groups at C-8). FsTRll6 mainly catalyzes esterification at C-8 of 3-ANEO to give 3-acetyl T-2 toxin (11) [58]. [Pg.3133]

Kotsonis, F. N., R. A. Ellison, and E. B. Smalley Isolation of acetyl T-2 toxin from Fusarium poae. Appl. Microbiol. 30, 493 (1975). [Pg.215]

Acetyl-T-2-toxin 3a,4)5,15-Triacetoxy-8a-(3-methylbutyryloxy)-12,13 epoxytrichothec-9-ene C26H36O10 Kotsonis et al. (1975)... [Pg.70]

Trichothecene 3-O-acetyltransferase encoded by a noncluster gene, TrilOl, readily converts isotrichodermol (130) into isotrichodermin (ITD, 131) (Figure 30).262 263 This acetylation step is important for the selfprotection of trichothecene-producing Fusarium species. The C-3 acetyl is also essential for subsequent biosynthetic steps to proceed. Indeed, the 7W/0/--targeted gene disruption mutant of F. sporotrichioides could not metabolize 3-hydroxytrichothecenes, but efficiently converted exogenously added ITD (131) and other C-3 acetylated intermediates into T-2 toxin.264 After ITD (131), the biosynthetic pathways are different between type A and type B trichothecenes. [Pg.441]

Trichothecenes can be divided into two groups based on their site of action on protein synthesis. Trichothecenes with hydroxyl and acetyl substitutions at both C-3 and C-4, such as T-2 toxin, DAS, verrucarin A, preferentially inhibit initiation while DON, trichodermin, crotocin, and verucarol inhibit elongation and/or termination (McLaughlin et al, 1977). Trichothecenes inhibit both DNA and RNA synthesis... [Pg.356]

The Tri3 gene of F. sporotrichioides encodes a 15-O-acetyl-trans-ferase that acetylates the 15-OH of 15-deacetylcalonectrin (117) (292). This enzyme also acetylates the 3o -hydroxyl in a number of 12,13-epoxytrichothecene substrates. The C-15 acetylation step appears to be essential to the pathway to T-2 toxin and Tri3 mutants accumulate neither T-2 toxin nor the major co-metabolites 4,15-diacetoxyscirpenol (121) and neosolaniol (128). [Pg.107]

Diacetoxyscirpenol (121), neosolaniol (128) and T-2 toxin (103) result from deacetylation of their respective 3-acetyl derivatives. [Pg.107]

Several surveys suggest that the most prevalent trichothecenes are deoxynivalenol (DON), nivalenol, 3-acetyl-DON (3-AcDON) and 15-acetyl-DON (15-AcDON), as type-B trichothecenes, and HT-2 toxin and T-2 toxin, as type-A trichothecenes. They are mainly found on maize, oats, barley, and wheat. The latter, espedally durum wheat, which is used nearly exclusively for the production of pasta, is susceptible to Fusaria infection and is often highly contaminated with DON. In European agricultural commodities type-A trichothecenes usually occur less frequently and at lower concentrations than DON. The simultaneous occurrence of DON with other Fusarium mycotoxins mainly type-B trichothecenes and zearalenone, has been reported for a variety of agricultural commodities (Gareis et al., 1989 Petterson, 1992, as cited in Krska et al., 2001). [Pg.227]

The specificity of monoclonal antibodies make it possible to develop an analytical method for a single mycotoxin, such as aflatoxin Bi in maize and groundnut meal, or aflatoxin Mj in milk and milk products. Even within chemically closely related structures such as the Fusarium trichothecenes there is very little cross-reactivity between a monoclonal raised to a single toxin such as T-2 toxin and other members of the family. Thus, a monoclonal raised against 3-acetyl-deoxynivalenol showed negligible cross-reactivity with deoxynivalenol, nivalenol, or T-2 toxin. [Pg.1514]

Kawai N, Yamagishi S, Saito M, Furuya K (1983) Blockade of synaptic transmission in the squid giant synapse by a spider toxin (JSTX). Brain Res 278 346-349 Kawai N, MiwaA, Shimazaki K, Sahara Y, Robinson HP, Nakajima T (1991) Spider toxin and the glutamate receptors. Comp Biochem Physiol C 98 87-96 Koike M, lino M, Ozawa S (1997) Blocking effect of 1-naphthyl acetyl spermine on Ca(2+)-permeable AMPA receptors in cultured rat hippocampal neurons. Neurosci Res 29 27-36... [Pg.211]


See other pages where Acetyl-T-2-toxin is mentioned: [Pg.294]    [Pg.226]    [Pg.158]    [Pg.75]    [Pg.294]    [Pg.226]    [Pg.158]    [Pg.75]    [Pg.103]    [Pg.441]    [Pg.445]    [Pg.58]    [Pg.664]    [Pg.146]    [Pg.107]    [Pg.107]    [Pg.109]    [Pg.238]    [Pg.250]    [Pg.252]    [Pg.3129]    [Pg.3131]    [Pg.3131]    [Pg.3133]    [Pg.3133]    [Pg.3144]    [Pg.964]    [Pg.49]    [Pg.337]    [Pg.69]    [Pg.149]   
See also in sourсe #XX -- [ Pg.158 ]

See also in sourсe #XX -- [ Pg.70 , Pg.75 ]




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