Toxic effects of T-2 toxin and deoxynivalenol on the mitochondrial electron transport system of cardiomyocytes in rats.
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The in vitro effects of 2 representative mycotoxins, T-2 toxin and deoxynivalenol (DON), of trichothecene group on the electron transport system (ETS) of mitochondria in rat cardiomyocytes were investigated by measuring oxygen consumption rates (OCR). The ATP-linked OCR and the reserve capacity (RC) of the mitochondria ETS were quantified by a "mitochondria stress test" which was estimated by the OCR responses to oligomycin and carbonyl cyanide-p-trifluoromethoxyphenylhydrazone, with an extracellular flux analyzer. The basal OCR was significantly inhibited by the application of T-2 toxin at concentrations of 6 x 10(-)(1) to 6 x 10(-)(5) muM and DON at concentrations of 0.78 to 100 muM for 24 hr. The threshold of cardiomyocyte toxicity was estimated to be between 6.0 x 10(-)(6) and 6.0 x 10(-)(5) muM for T-2 toxicity on both ATP-linked OCR and RC and between 0.39 and 0.78 muM on ATP-linked OCR or between 1.56 and 3.13 muM on RC for DON. The decrease in OCR of cardiomyocytes exposed to T-2 toxin with a concentration of 6.0 x 10(-)(3) and 6.0 x 10(-)(4) muM was significantly inhibited by antioxidants, catalase and vitamin C. In conclusion, the present study demonstrated, through the direct and real-time measurement of respiratory function in mitochondria, that a marked inhibition of mitochondrial ETS function in cardiomyocytes was induced by T-2 toxin and DON and that the mitochondrial dysfunction by T-2 toxin was largely associated with oxidative stress. (+info)
Development and evaluation of monoclonal antibodies for the glucoside of T-2 toxin (t2-glc).
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Toxicity of mycotoxins for the rat pulmonary macrophage in vitro.
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The presence of mycotoxins in grains is well documented. Workers in grain handling occupations are commonly exposed to grain dust aerosols. Work in our laboratory has shown that T-2 toxin is highly toxic to rat alveolar macrophages in vitro, causing loss of viability, release of radiolabeled chromium, inhibition of macromolecular synthesis, inhibition of phagocytosis, and inhibition of macrophage activation. Similarly, patulin caused a significant release of radiolabeled chromium, decrease in ATP levels, significant inhibition of protein and RNA synthesis, and inhibition of phagocytosis. The data show that both T-2 toxin and patulin are highly toxic to rat alveolar macrophages in vitro. The data further suggest that the presence of these mycotoxins in airborne respirable dust might present a hazard to exposed workers. (+info)
Effect of T-2 toxin on brain biogenic monoamines in rats and chickens.
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Two experiments were conducted to determine the effect of T-2 toxin on brain biogenic monoamines and their metabolites. Male rats (180 g) and cockerels (28 day, 300 g) were orally dosed with T-2 toxin at 2.5 mg kg-1 body weight. In the first experiment, whole brains were collected 2, 6, 12, 24 and 48 h postdosing and analyzed for monoamines by high performance liquid chromatography with electro-chemical detection. T-2 toxin did not influence whole brain concentrations of monoamines in either species. In the second experiment, brains were collected 24 h postdosing, dissected into five brain regions, and analyzed for monoamines. T-2 toxin treatment resulted in increased serotonin and 5-hydroxy-3-indoleacetic acid in all brain regions of the rat. However, this was not seen in poultry where T-2 toxin treatment resulted in an increase in 5-hydroxy-3-indoleacetic acid, no alteration in serotonin concentration and a decrease in regional norepinephrine and dopamine concentrations. These results suggest that T-2 toxin influences brain biogenic amine metabolism and that there is an intraspecies difference in the central effects of this mycotoxin. (+info)
In vitro and in vivo toxicity of T-2 toxin, a Fusarium mycotoxin, to mouse peritoneal macrophages.
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The effects of T-2 toxin on mouse peritoneal macrophages were investigated. Scanning electron microscopy of macrophages treated in vitro with T-2 toxin revealed retraction of pseudopodia. Protein synthesis was inhibited after in vitro contact with T-2 toxin but was not affected 24 h after injection of a sublethal dose of toxin into mice. There was reduction in the phagocytosis of Pseudomonas aeruginosa when macrophages were exposed in vitro to T-2 toxin and when mice were injected with T-2 toxin. Clearance of colloidal carbon was not modified after T-2 toxin injection, whereas spleen weight was decreased 24 h after T-2 injection. T-2 toxin enhanced the mortality of mice infected with Salmonella typhimurium C5S when it was administered 24 h prior to oral challenge with the bacterium. (+info)
Biotransformation and detoxification of T-2 toxin by soil and freshwater bacteria.
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Bacterial communities isolated from 17 of 20 samples of soils and waters with widely diverse geographical origins utilized T-2 toxin as a sole source of carbon and energy for growth. These isolates readily detoxified T-2 toxin as assessed by a Rhodotorula rubra bioassay. The major degradation pathway of T-2 toxin in the majority of isolates involved side chain cleavage of acetyl moieties to produce HT-2 toxin and T-2 triol. A minor degradation pathway of T-2 toxin that involved conversion to neosolaniol and thence to 4-deacetyl neosolaniol was also detected. Some bacterial communities had the capacity to further degrade the T-2 triol or 4-deacetyl neosolaniol to T-2 tetraol. Two communities, TS4 and KS10, degraded the trichothecene nucleus within 24 to 48 h. These bacterial communities comprised 9 distinct species each. Community KS10 contained 3 primary transformers which were able to cleave acetate from T-2 toxin but which could not assimilate the side chain products, whereas community TS4 contained 3 primary transformers which were able to grow on the cleavage products, acetate and isovalerate. A third community, AS1, was much simpler in structure and contained only two bacterial species, one of which transformed T-2 toxin to T-2 triol in monoculture. In all cases, the complete communities were more active against T-2 toxin in terms of rates of degradation than any single bacterial component. Cometabolic interactions between species is suggested as a significant factor in T-2 toxin degradation. (+info)