T-2 mycotoxin inhibits mitochondrial protein synthesis

Pace, J.; Watts, Michael R.; Canterbury, W J

doi:10.1016/0041-0101(88)90139-0

Cited by 58 publications

(21 citation statements)

References 27 publications

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“…The amphophilic nature of trichothecenes facilitates their cytotoxic effect on cell membranes (McLean 1996). Once trichothecenes cross the plasma membrane barrier, they enter the cell, where they can interact with a number of targets, including ribosome (McLaughlin et al 1977) and mitochondria (Pace et al 1988). Protein synthesis inhibition is the primary toxic effect of trichothecenes.…”

Section: Discussionmentioning

confidence: 99%

“…In a bovine kidney cell line, the mitocondrial activity was reduced after treatment with T-2 toxin (Holt et al 1988). In vitro, low concentrations of T-2 toxin resulted in a 50% inhibition of mitocondrial protein synthesis in rat liver cells (Pace et al 1988). T-2 toxin also inhibit electron transport activity in rat liver cells (Pace et al 1983) as suggested by the in vitro inhibition of succinic dehydrogenase activity and mitochondrial protein synthesis in rat hepatocytes (Trusal and O'Brien 1986).…”

Section: Effect On Cell Membrane and Organellesmentioning

confidence: 99%

“…Once trichothecenes cross the plasma membrane barrier, they enter the cell, where they can interact with a number of targets, including ribosome (McLaughlin et al 1977) and mitochondria (Pace et al 1988). Trichothecenes inhibit mitocondrial function in vivo and in vitro.…”

Section: Effect On Cell Membrane and Organellesmentioning

confidence: 99%

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Effects of trichothecene mycotoxins on eukaryotic cells: A review

Rocha

Ansari²,

Doohan³

2005

Food Additives and Contaminants

501

298

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The major products of the trichothecene mycotoxin biosynthetic pathway produced in a species-and sometimes isolatespecific manner by cereal-pathogenic Fusarium fungi include T-2 toxin, diacetoxyscirpenol, deoxynivalenol and nivalenol. This paper briefly reviews the major effects of such trichothecenes on the gross morphology, cytology and molecular signalling within eukaryotic cells. The gross toxic effects of select trichothecenes on animals include growth retardation, reduced ovarian function and reproductive disorders, immuno-compromization, feed refusal and vomiting. The phytotoxic effects of deoxynivalenol on plants can be summarized as growth retardation, inhibition of seedling and green plant regeneration. Trichothecenes are now recognized as having multiple inhibitory effects on eukaryote cells, including inhibition of protein, DNA and RNA synthesis, inhibition of mitochondrial function, effects on cell division and membrane effects. In animal cells, they induce apoptosis, a programmed cell death response. Current knowledge about the eukaryotic signal transduction cascades and downstream gene products activated by trichothecenes is limited, especially in plants. In mammalian cells, certain trichothecenes trigger a ribotoxic stress response and activate mitogen-activated protein kinases. DON mediates the inflammatory response by modulating the binding activities of specific transcription factors and subsequently inducing cytokine gene expression. Several genes are up-regulated in wheat in response to trichothecene mycotoxins; the significance, if any, of these genes in the host response to trichothecenes has yet to be elucidated.

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Section: Discussionmentioning

confidence: 99%

Section: Effect On Cell Membrane and Organellesmentioning

confidence: 99%

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Effects of trichothecene mycotoxins on eukaryotic cells: A review

Rocha

Ansari²,

Doohan³

2005

Food Additives and Contaminants

501

298

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“…These observations suggest that toxicity of trichothecenes might not be a simple function of translational arrest and that they may have multiple mechanisms of toxicity. Despite the early studies that implicated DNA synthesis (2), respiration (17), mitochondrial protein synthesis (17), and membrane structure and integrity (18) in the cytotoxicity of trichothecenes, the molecular mechanisms of their toxicity are not well understood, and the proteins targeted by trichothecenes other than L3 have not been identified. To develop a better understanding of the trichothecene mechanism of action, we used a chemical genomics approach in S. cerevisiae to identify genes that when deleted confer resistance to trichothecin (Tcin).…”

mentioning

confidence: 99%

A genome-wide screen in Saccharomyces cerevisiae reveals a critical role for the mitochondria in the toxicity of a trichothecene mycotoxin

McLaughlin

Bin-Umer

Tortora

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Trichothecene mycotoxins synthesized by Fusarium species are potent inhibitors of eukaryotic translation. They are encountered in both the environment and in food, posing a threat to human and animal health. They have diverse roles in the cell that are not limited to the inhibition of protein synthesis. To understand the trichothecene mechanism of action, we screened the yeast knockout library to identify genes whose deletion confers resistance to trichothecin (Tcin). The largest group of resistant strains affected mitochondrial function, suggesting a role for fully active mitochondria in trichothecene toxicity. Tcin inhibited mitochondrial translation in the wild-type strain to a greater extent than in the most resistant strains, implicating mitochondrial translation as a previously unrecognized site of action. The Tcin-resistant strains were cross-resistant to anisomycin and chloramphenicol, suggesting that Tcin targets the peptidyltransferase center of mitochondrial ribosomes. Tcin-induced cell death was partially rescued by mutants that regulate mitochondrial fusion and maintenance of the tubular morphology of mitochondria. Treatment of yeast cells with Tcin led to the fragmentation of the tubular mitochondrial network, supporting a role for Tcin in disruption of mitochondrial membrane morphology. These results provide genome-wide insight into the mode of action of trichothecene mycotoxins and uncover a critical role for mitochondrial translation and membrane maintenance in their toxicity.Fusarium head blight ͉ ribosome ͉ translation ͉ deoxynivalenol ͉ mycotoxin

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“…It is responsible for the inhibition of the synthesis of proteins and DNA synthetase in eukaryotic cells [72]. T-2 is usually present in the cereals like oats, barley and wheat [73].…”

Section: (2) (2017) 84-95mentioning

confidence: 99%

A review of the presence of some food contaminants on the territory of the Republic of Serbia

Danilović¹,

Potić²,

Stamenković³

et al. 2017

Adv Techol

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Food contamination is one of the major problems in food distribution. Microorganisms and their metabolites are the most common food contaminants. This review consolidates the reported food contamination cases in the Republic of Serbia. Mycotoxins were stated as the most common contaminants in various foods. Among them mycotoxins like zearalenone, aflatoxins, fumonisins, and deoxynivalenol were the most frequently detected. Also, the contamination caused by the presence of various microorganisms like L. monocytogenes, E. coli, Salmonella spp. and S. aureus was reported in high frequency. The microbial contamination was usually detected in meat and dairy products. Although heavy metals were detected in some products, in most cases their concentrations were in accordance with the legislation. A higher level of Pb and Hg was stated only in a few samples of tea, milk and fish. The constant analysis, control and prevention are needed at all levels of the production in order to compile the safety requirements and international legislation.

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T-2 mycotoxin inhibits mitochondrial protein synthesis

Cited by 58 publications

References 27 publications

Effects of trichothecene mycotoxins on eukaryotic cells: A review

Effects of trichothecene mycotoxins on eukaryotic cells: A review

A genome-wide screen in Saccharomyces cerevisiae reveals a critical role for the mitochondria in the toxicity of a trichothecene mycotoxin

A review of the presence of some food contaminants on the territory of the Republic of Serbia

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