Supplementary Data on Crotocin—an Antifungal Antibiotic

Gláz, E; Csányi, Erzsébet; Gyimesi, J.

doi:10.1038/212617b0

Cited by 24 publications

(3 citation statements)

References 6 publications

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“…Little is known about the mechanism of action and the effects of type C trichothecenes such as crotocin on the cell and/or organs, only three papers on the topic are referenced in PubMed (Glaz et al, 1966, Liao et al, 1976, Chi and Mirocha, 1978. Like other trichothecenes, crotocin inhibits protein synthesis through ribotoxic action in HeLa cells, but no information is available regarding the possible involvement of oxidative stress in the effect of this toxin on cells.…”

Section: Toxicological Effects Of Type C Trichothecenesmentioning

confidence: 99%

Review article: Role of satiety hormones in anorexia induction by Trichothecene mycotoxins

Terciolo

Maresca

Pinton

et al. 2018

Food and Chemical Toxicology

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The trichothecenes, produced by Fusarium, contaminate animal feed and human food in all stages of production and lead to a large spectrum of adverse effects for animal and human health. An hallmark of trichothecenes toxicity is the onset of emesis followed by anorexia and food intake reduction in different animal species (mink, mice and pig). The modulation of emesis and anorexia can result from a direct action of trichothecenes in the brain or from an indirect action in the gastrointestinal tract. The direct action of trichothecenes involved specific brain areas such as nucleate tractus solitarius in the brainstem and the arcuate nuclei in the hypothalamus. Activation of these areas in the brain leads to the activation of specific neuronal populations containing anorexigenic factors (POMC and CART). The indirect action of trichothecenes in the gastrointestinal tract involved, by enteroendocrine cells, the secretion of several gut hormones such as cholecystokinin (CCK) and peptide YY (PYY) but also glucagon-like peptide 1 (GLP-1), gastric inhibitory peptide (GIP) and 5hydroxytryptamine (5-HT), which transmitted signals to the brain via the gut-brain axis. This review summarizes current knowledge on the effects of trichothecenes, especially deoxynivalenol, on emesis and anorexia and discusses the mechanisms underlying trichothecenes-induced food reduction.

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Section: Toxicological Effects Of Type C Trichothecenesmentioning

confidence: 99%

Review article: Role of satiety hormones in anorexia induction by Trichothecene mycotoxins

Terciolo

Maresca

Pinton

et al. 2018

Food and Chemical Toxicology

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“…The trichothecen-&one -+ 7,13-cyclotrichothecenone rearrangement. The 12,13-epoxide of trichothecolone ( 89) is attacked by the 7-carbanion that can be generated in boiling 1 M sodium hydroxide, giving isotrichothecolone (90). Since the nature of this reaction was e l ~c i d a t e d , ' ~~ no further examples have been described.…”

Section: 421mentioning

confidence: 99%

Non-macrocyclic trichothecenes

Grove¹

1988

Nat. Prod. Rep.

137

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“…These compounds are generally highly toxic to animals and plants and have been identified as significant toxic agents in numerous medically and economically important mycotoxicoses afflicting man and domestic animals (2)(3)(4)(5)(6)(7)(8)(9)(10). Aside from their toxicity to eukaryotes, the 12,13-epoxytrichothecenes are of interest because several possess antineoplastic activity (11,12).…”

mentioning

confidence: 99%

Mechanism of Action of the Mycotoxin Trichodermin, a 12,13-Epoxytrichothecene

Wei

Hansen

Vaughan

et al. 1974

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

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Trichodermin is a member of a group of closely related compounds-the 12,13-epoxytrichothecenes-that form a medically and economically important class of mycotoxins produced by fungi that spoil fruit and grain. Our studies show that trichodermin is a very potent inhibitor of protein synthesis in mammalian cells. Since ribosomes remain in polyribosomes in inhibited cells, trichodermin inhibits the elongation and/or termination processes of protein synthesis. In vitro, trichodermin is a potent inhibitor of the peptidyl transferase activity required for elongation and/or termination. An in vitro comparison of the effects of three peptidyl transferase inhibitors on elongation and termination indicates that anisomycin acts primarily on elongation while trichodermin and sparsomycin act primarily on termination. A new in vivo test to distinguish elongation inhibitors from termination inhibitors confirms that trichodermin inhibits primarily the termination process. Thus trichodermin inhibits protein synthesis by blocking the activity of peptidyl transferase required for termination. These studies suggest that the toxicosis caused by one of the 12,13-epoxytrichothecenes is due to its action as a protein synthesis inhibitor involving the peptidyl transferase activity of the eukaryotic ribosomes.

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Supplementary Data on Crotocin—an Antifungal Antibiotic

Cited by 24 publications

References 6 publications

Review article: Role of satiety hormones in anorexia induction by Trichothecene mycotoxins

Review article: Role of satiety hormones in anorexia induction by Trichothecene mycotoxins

Non-macrocyclic trichothecenes

Mechanism of Action of the Mycotoxin Trichodermin, a 12,13-Epoxytrichothecene

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