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Biomedical subjects

B Yagen

Publications and source records attributed to B Yagen.

88 records · Page 5Linked to original sources
PubMed1977

Comparative study of the yield of T-2 toxic produced by Fusarium poae, F. sporotrichioides and F. sporotrichioides var. tricinctum strains from different sources.

Eleven strains of Fusarium poae and F. sporotrichioides from the U.S.S.R. and 7 strains of these species and one of F. sporotrichioides var. tricinctum from U.S.A. and France have been compared as to their capacity to yield T-2 toxin. The presence of this toxin was confirmed by thin layer chromatography, gas liquid chromatography and mass spectroscopy. The strains which came from the U.S.S.R. and were originally involved in causing Alimentary Toxic Aleukia (ATA), produced several times more T-2 toxin than the others. We assume that the ability of the U.S.S.R. strains to produce much more T-toxin is due to the different ecological conditions under which they were first isolated. The remarkable maintenance of so high a level of toxin production over more than 30 years of culturing is worthy of note.

Animals↗
PubMed1976

Screeing of toxic isolates of Fusarium poae and Fusarium sporotrichiodes involved in causing alimentary toxic aleukia.

A total of 131 isolates of Fusarium poae and F. sporotrichioides from overwintered cereals, which were associated with the alimentary toxic aleukia toxicoses in the Soviet Union, were tested for their ability to produce T-2 toxin [4 beta, 15 diacetoxy-8alpha-(3-methylbutyryloxy)-12,13-epoxytrichothec-9-en 3alpha-ol]. The presence of T-2 toxin was determined by thin-layer chromatography, gas-liquid chromatography, spectroscopic analyses, and the rabbit skin test. A good correlation was demonstrated between T-2 toxin dectetion by thin-layer chromatography and inflammatory skin reactions of rabbits.

Animals↗
PubMedDate not supplied

T-2 toxin effect on isolated perfused rat hearts.

T-2 toxin is the major lethal component of several Fusarium fungi implicated in the disease of man and animals. We used isolated rats hearts to test the T-2 toxin cardiotoxicity. Electrodynamics and ultrastructural parameters were studied. The main changes consisted of decreased contractility and electrocardiographic abnormalities without much effect on heart rate or QRS and QT intervals. Ultrastructurally, swelling of myofibers and their mitochondria occurred and damage to the plasma membrane was seen. It is possible that the T-2 effect is mediated through soluble thiol to cause cytoplasmic calcium decrease and loss of plasma membrane integrity.

Animals↗
PubMedDate not supplied

Mycotoxicosis caused by either T-2 toxin or diacetoxyscirpenol in the diet of broiler chickens.

Seven-day-old male broiler chickens were fed either T-2 toxin or diacetoxyscirpenol at 4 and 16 ppm for 21 days and had reductions of feed consumption and of weight gain. Focal, yellow, oral plaques developed by day 2 and were located around salivary duct openings on the palate, tongue, and buccal floor. The plaques progressed to raised, yellowish-gray crusts which covered ulcers. Microscopically, the ulcers had a base of granulation tissue and inflammatory cells, and the crusts comprised exudate, bacterial colonies and feed components. T-2 toxin and diacetoxyscirpenol produced similar effects at these concentrations. Comparable lesions also occurred in chickens fed T-2 toxin at 50, 100, or 300 ppm for 7 days. Six of 10 chickens died in the 300-ppm group which received an average daily exposure of about 10 mg T-2 toxin/kg body weight. In dead chickens, the lymphoid and hematopoietic tissues and alimentary mucosa were necrotic. Necrosis was seen less frequently in the liver, kidney and the feather. Survivors of the 7-day studies had atrophied lymphoid organs and were anemic.

Animal Feed↗
PubMedDate not supplied

Pharmacokinetics of T-2 toxin and its metabolite HT-2 toxin, after intravenous administration in dogs.

The pharmacokinetics of T-2 toxin and HT-2 toxin were investigated comparatively in five dogs, after iv administration of the toxins (0.4 mg/kg). T-2 toxin was very rapidly and almost completely biotransformed to HT-2 toxin (fm = 83.6 +/- 3.9%). The following mean pharmacokinetic parameters were determined in this study for T-2 toxin and HT-2 toxin, respectively: half-life 5.3 +/- 2.1 and 19.6 +/- 4.7 min, clearance 0.107 +/- 0.056 and 0.167 +/- 0.074 liters/min/kg, and volume of distribution 0.86 +/- 0.63 and 4.47 +/- 1.38 liters/kg. The high clearance values suggest that the metabolism of T-2 toxin and HT-2 toxin is carried out in blood and/or through diffusion by nonspecific carboxyesterases. The results of this study suggest the possibility of a sustenance of T-2 toxin metabolism by its binding to blood cells.

Animals↗
PubMedDate not supplied

The metabolism and excretion of 14C-styrene oxide-glutathione adducts administered to the winter flounder, Pseudopleuronectes americanus, a marine teleost. Identification of the corresponding S-cysteine derivatives as major urinary metabolites.

The metabolism and excretion of intramuscularly administered 14C-glutathione conjugates of styrene oxide (Ia and IIa) were studied in the winter flounder at three dose levels. The various radiolabeled thioether metabolites excreted were separated by reverse-phase high pressure liquid chromatography, and identified and quantitated by cochromatography with synthetic standards. The urine was the major excretion route for radioactivity derived from the glutathione conjugates (up to 90%) at each dose level (1.0, 3.9, and 24.4 mg/fish) studied. The corresponding cysteine derivatives (Ic, IIc) were the major urinary metabolites although the N-acetylcysteine derivatives (Id, IId), or mercapturic acids, were also present in significant amounts at each dose and excretion interval examined. Unchanged glutathione conjugates of styrene oxide were the major radioactive constituents of 24-hr bile samples from the treated flounder, although significant amounts of the cysteinylglycine (Ib, IIb), cysteine, and N-acetylcysteine derivatives were also present in bile. Bile was a minor excretory route relative to urine. The oxidation of 14C-styrene to styrene 7,8-oxide by the cytochrome P-450-dependent monooxygenase system of hepatic microsomes of winter flounder was also demonstrated; likewise, styrene was converted to the diastereomeric glutathione conjugates of styrene 7,8-oxide by 9,000g supernatant fractions of flounder liver supplemented with glutathione. This study demonstrated that flounder liver can convert styrene to glutathione conjugates to styrene oxide and that mercapturic acid biosynthesis occurs after parenteral administration of a xenobiotic-glutathione adduct to this marine species, although the major urinary metabolites were the cysteine conjugates rather than the anticipated mercapturic acid derivatives.

Acetylcysteine↗