Detection of macrocyclic trichothecene mycotoxin in acaprine(goat) tracheal instillation model

2009 ◽  
Vol 25 (9-10) ◽  
pp. 693-701 ◽  
Author(s):  
Robert C Layton ◽  
Charles W Purdy ◽  
Cynthia A Jumper ◽  
David C Straus
Keyword(s):  
Trichothecene Mycotoxin ◽  
Macrocyclic Trichothecene

Conformational properties of the macrocyclic trichothecene mycotoxin verrucarin A in solution

2008 ◽  
Vol 46 (12) ◽  
pp. 1102-1111 ◽  
Author(s):  
Georgia Fragaki ◽  
Irine Stefanaki ◽  
Photis Dais ◽  
Emmanuel Mikros
Keyword(s):  
Trichothecene Mycotoxin ◽  
Conformational Properties ◽  
Macrocyclic Trichothecene

Neurotoxic, Inflammatory, and Mucosecretory Responses in the Nasal Airways of Mice Repeatedly Exposed to the Macrocyclic Trichothecene Mycotoxin Roridin A

2010 ◽  
Vol 38 (3) ◽  
pp. 429-451 ◽  
Author(s):  
Kara N. Corps ◽  
Zahidul Islam ◽  
James J. Pestka ◽  
Jack R. Harkema
Keyword(s):  
Upper Respiratory Tract ◽  
Trichothecene Mycotoxin ◽  
Mucus Hypersecretion ◽  
Nasal Airways ◽  
Adverse Health Effects ◽  
Morphometric Analyses ◽  
Effect Level ◽  
Nasal Inflammation ◽  
Dose Dependent ◽  
Macrocyclic Trichothecene

Macrocyclic trichothecene mycotoxins encountered in water-damaged buildings have been suggested to contribute to illnesses of the upper respiratory tract. Here, the authors characterized the adverse effects of repeated exposures to roridin A (RA), a representative macrocyclic trichothecene, on the nasal airways of mice and assessed the persistence of these effects. Young, adult, female C57BL/6 mice were exposed to single daily, intranasal, instillations of RA (0.4, 2, 10, or 50 μg/kg body weight [bw]) in saline (50 μl) or saline alone (controls) over 3 weeks or 250 μg/kg RA over 2 weeks. Histopathologic, immunohistochemical, and morphometric analyses of nasal airways conducted 24 hr after the last instillation revealed that the lowest-effect level was 10 μg/kg bw. RA exposure induced a dose-dependent, neutrophilic rhinitis with mucus hypersecretion, atrophy and exfoliation of nasal transitional and respiratory epithelium, olfactory epithelial atrophy and loss of olfactory sensory neurons (OSNs). In a second study, the persistence of lesions in mice instilled with 250 μg/kg bw RA was assessed. Nasal inflammation and excess luminal mucus were resolved after 3 weeks, but OSN loss was still evident in olfactory epithelium (OE). These results suggest that nasal inflammation, mucus hypersecretion, and olfactory neurotoxicity could be important adverse health effects associated with short-term, repeated, airborne exposures to macrocyclic trichothecenes.

Prepubertal exposure to T-2 toxin advances pubertal onset and development in female rats via promoting the onset of hypothalamic–pituitary–gonadal axis function

2016 ◽  
Vol 35 (12) ◽  
pp. 1276-1285 ◽  
Author(s):  
R Yang ◽  
Y-M Wang ◽  
L Zhang ◽  
Z-M Zhao ◽  
J Zhao ◽  
...  
Keyword(s):  
Messenger Rna ◽  
Female Rats ◽  
Intragastric Administration ◽  
Corpora Lutea ◽  
Sprague Dawley ◽  
Trichothecene Mycotoxin ◽  
Pubertal Onset ◽  
Serum Hormone ◽  
Puberty Onset ◽  
High Level

T-2 toxin, a naturally produced Type A trichothecene mycotoxin, has been shown to damage the reproductive and developmental functions in livestocks. However, whether T-2 toxin can disturb the pubertal onset and development following prepubertal exposure remains unclear. To clarify this point, infantile female Sprague–Dawley rats were given a daily intragastric administration of vehicle or T-2 toxin at a dose of 375 μg/kg body weight for 5 consecutive days from postnatal day (PND) 15–19 (PND15–PND19). The days of vaginal opening, first diestrus, and first estrus in regular estrous cycle were advanced following T-2 toxin treatment, indicating prepubertal exposure to T-2 toxin induced the advancement of puberty onset. The relative weights of uterus and ovaries and the incidence of corpora lutea were all increased in T-2 toxin-treated rats; serum hormone levels of luteinizing hormone and estradiol and the messenger RNA expressions of gonadotropin-releasing hormone (GnRH) and GnRH receptor also displayed marked increases following exposure to T-2 toxin, all of which were well consistent with the manifestations of the advanced puberty onset. In conclusion, the present study reveals that prepubertal exposure to a high level of T-2 toxin promotes puberty onset in infantile female rats by advancing the initiation of hypothalamic–pituitary–gonadal axis function in female rats.

scholarly journals Antifungal Activity of Phenyl Derivative of Pyranocoumarin fromPsoralea corylifoliaL. Seeds by Inhibition of Acetylation Activity of Trichothecene 3-O-Acetyltransferase (Tri101)

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Sangeetha Srinivasan ◽  
D. V. L. Sarada
Keyword(s):  
Hydrogen Bond ◽  
Antifungal Activity ◽  
Defense Mechanism ◽  
Petroleum Ether Extract ◽  
Ligand Docking ◽  
Molecular Formula ◽  
Trichothecene Mycotoxin ◽  
Hydrogen Bond Interaction ◽  
Phenyl Derivative ◽  
Bond Interaction

Antifungal activity of petroleum ether extract ofPsoralea corylifoliaL. seed, tested againstFusariumsp. namely,Fusarium oxysporum, Fusarium moniliforme,andFusarium graminearum, was evaluated by agar well diffusion assay. The chromatographic fractionation of the extract yielded a new phenyl derivative of pyranocoumarin (PDP). The structure of the PDP was confirmed using spectroscopic characterization (GC-MS, IR, and NMR), and a molecular mass ofm/z414 [M-2H]+with molecular formula C27H28O4was obtained. The PDP had a potent antifungal activity with a minimum inhibitory concentration of 1 mg/mL againstFusariumsp. Molecular docking using Grid-Based Ligand Docking with Energetics (GLIDE, Schrodinger) was carried out with the Tri101, trichothecene 3-O-acetyltransferase, as target protein to propose a mechanism for the antifungal activity. The ligand PDP showed bifurcated hydrogen bond interaction with active site residues at TYR 413 and a single hydrogen bond interaction at ARG 402 with a docking score −7.19 and glide energy of −45.78 kcal/mol. This indicated a strong binding of the ligand with the trichothecene 3-O-acetyltransferase, preventing as a result the acetylation of the trichothecene mycotoxin and destruction of the “self-defense mechanism” of theFusariumsp.

scholarly journals The Effect of HT-2 Toxin on Ovarian Steroidogenesis and Its Response to IGF-I, Leptin and Ghrelin in Rabbits

2017 ◽  
pp. 705-708 ◽  
Author(s):  
A. KOLESAROVA ◽  
N. MARUNIAKOVA ◽  
A. KADASI ◽  
M. HALENAR ◽  
M. MARAK ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fusarium Species ◽  
Endocrine System ◽  
Control Group ◽  
Trichothecene Mycotoxin ◽  
Ovarian Steroidogenesis ◽  
Estradiol Secretion ◽  
Igf I ◽  
17Β Estradiol

T-2 toxin and its metabolite HT-2 toxin are one of the most toxic mycotoxins of type A-trichothecenes, which are produced mainly by Fusarium species. Therefore, study of Fusarium toxins T-2 toxin and HT-2 toxin is an essential issue because they could also play role in failures of reproductive functions as well as endocrine system of domestic animals. Assessment of the effect of A-trichothecene mycotoxin HT-2 toxin alone or combined with insulin-like growth factor (IGF-I), leptin and ghrelin on estradiol secretion by rabbit ovarian fragments in vitro was done. Rabbit ovarian fragments were incubated without (control group) or with HT-2 toxin, or its combinations with IGF-I, leptin and ghrelin at various concentrations for 24 h. Secretion of 17β-estradiol was determined by ELISA. Firstly, HT-2 toxin at the doses 10 and 100 ng.ml-1, but not at 1 ng.ml-1 decreased 17β-estradiol secretion by ovarian fragments. Secondly, 17β-estradiol secretion was not affected by HT-2 toxin exposure combined with growth factor IGF-I, metabolic hormones leptin and ghrelin. In conclusion, HT-2 toxin has potent direct dose-dependent effects on ovarian steroidogenesis in rabbits. These direct effects of HT-2 mycotoxin on ovarian steroidogenesis could impact negatively on the reproductive performance of rabbits.

Catalytic NBP Spot Test for the Detection of Trichothecene Mycotoxin T-2

1986 ◽  
Vol 19 (19-20) ◽  
pp. 2001-2009 ◽  
Author(s):  
Thaddeus J. Novak ◽  
Karen A. Quinn
Keyword(s):  
Spot Test ◽  
Trichothecene Mycotoxin

scholarly journals Expression of a Truncated Form of Ribosomal Protein L3 Confers Resistance to Pokeweed Antiviral Protein and the Fusarium Mycotoxin Deoxynivalenol

2005 ◽  
Vol 18 (8) ◽  
pp. 762-770 ◽  
Author(s):  
Rong Di ◽  
Nilgun E. Tumer
Keyword(s):  
Ribosomal Protein ◽  
Fusarium Species ◽  
Common Mechanism ◽  
Pokeweed Antiviral Protein ◽  
Wild Type ◽  
Antiviral Protein ◽  
Trichothecene Mycotoxin ◽  
Truncated Form ◽  
Fusarium Mycotoxin ◽  
Ribosomal Protein L3

The contamination of important agricultural products such as wheat, barley, or maize with the trichothecene mycotoxin deoxynivalenol (DON) due to infection with Fusarium species is a worldwide problem. Trichothecenes inhibit protein synthesis by targeting ribosomal protein L3. Pokeweed antiviral protein (PAP), a ribosome-inactivating protein binds to L3 to depurinate the α–sarcin/loop of the large rRNA. Plants transformed with the wild-type PAP show lesions and express very low levels of PAP because PAP autoregulates its expression by destabilizing its own mRNA. We show here that transgenic tobacco plants expressing both the wild-type PAP and a truncated form of yeast L3 (L3δ) are phenotypically normal. PAP mRNA and protein levels are very high in these plants, indicating that L3δ suppresses the autoregulation of PAP mRNA expression. Ribosomes are not depurinated in the transgenic plants expressing PAP and L3δ, even though PAP is associated with ribosomes. The expression of the endogenous tobacco ribosomal protein L3 is up-regulated in these plants and they are resistant to the Fusarium mycotoxin DON. These results demonstrate that expression of an N-terminal fragment of yeast L3 leads to trans-dominant resistance to PAP and the trichothecene mycotoxin DON, providing evidence that both toxins target L3 by a common mechanism.

Sign in / Sign up

Export Citation Format

Share Document