Effects of the Fusarium toxin deoxynivalenol on tissue protein synthesis in pigs

Dänicke, Sven; Goyarts, Tanja; Döll, Susanne; Grove, Nicola; Spolders, Markus; Flachowsky, Gerhard

doi:10.1016/j.toxlet.2006.05.006

Cited by 75 publications

(48 citation statements)

References 45 publications

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“…The results represent the mean bacterial count per macrophages ± standard error of the mean (sem) after invasion (0 h) and after proliferation (6 h), as well as the proliferation rate. on the dietary content of DON, serum concentrations of DON varying from 0.013 to 0.026 lg/mL were measured in pigs [9,19]. The growth of Salmonella Typhimurium was not affected by concentrations of DON up to 50 lg/mL.…”

Section: Don Induced Cell Morphology Changesmentioning

confidence: 99%

The mycotoxin deoxynivalenol promotes uptake ofSalmonellaTyphimurium in porcine macrophages, associated with ERK1/2 induced cytoskeleton reorganization

Vandenbroucke¹,

Croubels²,

Verbrugghe³

et al. 2009

Vet. Res.

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-Both the mycotoxin deoxynivalenol (DON) and Salmonella Typhimurium are major issues in swine production. This study aimed at examining the interaction between DON and Salmonella Typhimurium at the level of the porcine innate immune system, represented by macrophages. First, we assessed the direct cytotoxic effect of DON on porcine macrophages. Incubation with 0.25 lg/mL of DON or higher resulted in a significant cytotoxic effect after 24 h of incubation. Secondly, the direct toxic effect of DON on the growth and on the expression of Salmonella pathogenicity island 1 (SPI-1) and SPI-2 virulence genes of Salmonella Typhimurium was determined. At low non-cytotoxic concentrations, as can be found in the serum of pigs, DON did not have any effect on either growth or virulence gene expression of Salmonella Typhimurium. However, when the invasion and intracellular survival of Salmonella Typhimurium in macrophages preexposed to 0.025 lg/mL of DON was examined, DON significantly promoted the uptake of Salmonella Typhimurium into macrophages. The enhanced uptake coincided with marked F-actin reorganization of the cells, which was due to the activation of extracellular signal-regulated protein kinase 1/2 (ERK1/2). These results suggest that low but relevant concentrations of DON modulate the innate immune system and could thus increase the susceptibility of pigs to infections with Salmonella Typhimurium.deoxynivalenol / Salmonella Typhimurium / pig / macrophage / cytoskeleton

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Section: Don Induced Cell Morphology Changesmentioning

confidence: 99%

The mycotoxin deoxynivalenol promotes uptake ofSalmonellaTyphimurium in porcine macrophages, associated with ERK1/2 induced cytoskeleton reorganization

Vandenbroucke¹,

Croubels²,

Verbrugghe³

et al. 2009

Vet. Res.

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show abstract

“…However, on the basis of previous reports (Bensassi et al, 2012;Ma et al, 2012), it is plausible that DON also exerts its toxicity through oxidative stress. Considering the overall mechanism of cytotoxic effects of DON and T-2 toxin, it is presumed that oxidative stress in addition to protein synthesis inhibition (Dänicke, 2006;Doi et al, 2008;Pestka, 2008) in cells is importantly involved.…”

Section: Figmentioning

confidence: 99%

Toxic effects of T-2 toxin and deoxynivalenol on the mitochondrial electron transport system of cardiomyocytes in rats

et al. 2013

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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 × 10 -1 to 6 × 10 -5 μM and DON at concentrations of 0.78 to 100 μM for 24 hr. The threshold of cardiomyocyte toxicity was estimated to be between 6.0 × 10 -6 and 6.0 × 10 -5 μM for T-2 toxicity on both ATP-linked OCR and RC and between 0.39 and 0.78 μM on ATP-linked OCR or between 1.56 and 3.13 μM on RC for DON. The decrease in OCR of cardiomyocytes exposed to T-2 toxin with a concentration of 6.0 × 10 -3 and 6.0 × 10 -4 μM 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.

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“…27,28) Since the Fusarium toxin deoxynivalenol is known to be a potent protein synthesis inhibitor according to the research in vitro and in vivo systems, it especially reduces proteins of the peripheral lymphocytes and serum protein secretion from the hepatocytes. 29,30) Moreover, reduced feed uptake with feed refusal as the adverse effect of DON can aggravate the protein synthesis efficiency. Therefore, translationally-disrupted apoprotein metabolism can retard the release of triglyceride lipoprotein into the circulation and result in fat accumulation as droplets in the liver cells.…”

Section: Effects Of Don Treatment On the Embryonic Splenic Lymphoprolmentioning

confidence: 99%

Toxic Alterations in Chick Embryonic Liver and Spleen by Acute Exposure to Fusarium-Producing Mycotoxin Deoxynivalenol

Moon

Kim²,

Suh

et al. 2007

Biological & Pharmaceutical Bulletin

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Food mycotoxin deoxynivalenol (vomitoxin, DON) produced by Fusarium graminearum and F. culmorum can induce rapid diminution of lymphoid tissues and lymphopenia in the growing chickens and mammals. We first investigated the direct acute effects of DON on the chick immune-related embryo tissues such as embryonic liver and spleen. Direct DON administration into the embryonic eggs caused toxin accumulation in liver in a time-dependent manner. Electron microscopic observation showed a notable accumulation of fat droplet in the liver tissue and the re-exposed hatched chicken showed more distinguishing enlarged fat globules, so-called fatty cysts like human steatosis. Regarding effects of deoxynivalenol on the chick embryonic spleen, fatty change was also observed in splenocytes. Functionally, mitogen-stimulated cellular and humoral lympho-proliferations were suppressed in the DON-treated embryo. Conclusively, acute direct exposure to deoxynivalenol in the chick embryo caused toxic histological alterations in the liver and spleen and suppressed in vitro lymphoblastogenesis.

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Effects of the Fusarium toxin deoxynivalenol on tissue protein synthesis in pigs

Cited by 75 publications

References 45 publications

The mycotoxin deoxynivalenol promotes uptake ofSalmonellaTyphimurium in porcine macrophages, associated with ERK1/2 induced cytoskeleton reorganization

The mycotoxin deoxynivalenol promotes uptake ofSalmonellaTyphimurium in porcine macrophages, associated with ERK1/2 induced cytoskeleton reorganization

Toxic effects of T-2 toxin and deoxynivalenol on the mitochondrial electron transport system of cardiomyocytes in rats

Toxic Alterations in Chick Embryonic Liver and Spleen by Acute Exposure to Fusarium-Producing Mycotoxin Deoxynivalenol

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