Report from SCOOP task 3.2.10 “collection of occurrence data of Fusarium toxins in food and assessment of dietary intake by the population of EU member states”

Schothorst, R.C.; Egmond, H. P. van

doi:10.1016/j.toxlet.2004.04.045

Cited by 270 publications

(141 citation statements)

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“…1), the trichothecenes nivalenol, will enhance the aflatoxin B1-induced hepatocarcinogenesis and T-2 lack any hepatocarcinogenesis ability and that was confirmed by an investigation in the presence of GST-P-positive foci that acts as a marker for the presence of hepatocarcinogenesis (203). Although it was proposed (204) that under the experimental conditions in both in vivo and in vitro, no damage took place in the hepatic DNA, T-2 has the ability to decrease responses to mitogens in human lymphocytes in vitro (205).…”

Section: Mycotoxins and Their Carcinogenicitymentioning

confidence: 90%

“…Nivalenol can also be involved in casing sister chromatid exchange in Chinese hamster cells and it can case DNA damage making it a potential genotoxic agent (205) which can be hypothesized in humans as well. Nivalenol acute toxicity can lead to bone marrow toxicity and Nivalenol chronic toxicity would lead to leucopenia (209).…”

Section: Mycotoxins and Their Carcinogenicitymentioning

confidence: 99%

“…Nivalenol acute toxicity can lead to bone marrow toxicity and Nivalenol chronic toxicity would lead to leucopenia (209). Unfortunately, there is no clear evidence of Nivalenol carcinogenicity in experimental animals or humans and an investigation was carried on cell lines in vitro (205,210).…”

Section: Mycotoxins and Their Carcinogenicitymentioning

confidence: 99%

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Effects of different mycotoxins on humans, cell genome and their involvement in cancer

et al. 2017

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Abstract. The chemical nature of most of the mycotoxins makes them highly liposoluble compounds that can be absorbed from the site of exposure such as from the gastrointestinal and respiratory tract to the blood stream where it can be dissimilated throughout the body and reach different organs such as the liver and kidneys. Mycotoxins have a strong tendency and ability to penetrate the human and animal cells and reach the cellular genome where it causes a major mutagenic change in the nucleotide sequence which leads to strong and permanent defects in the genome. This defect will eventually be transcribed, translated and lead to the development of cancer. In this review, the chemical and physical nature of mycotoxins, the action of mycotoxins on the cellular genome and its effect on humans, mycotoxins and their carcinogenicity and mycotoxins research gaps are discussed, and new research areas are suggested. The research review posed various questions. What are the different mycotoxins that can cause cancer, what is the role of mycotoxins in causing cancer and what types of cancers can be caused by mycotoxins? These questions have been selected due to the significant increase in the mycotoxin contamination and the cancer incidence rate in the contemporary world. By revealing and understanding the role of mycotoxins in developing cancer, measures to reduce the risks and incidents of cancer could be taken.

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Section: Mycotoxins and Their Carcinogenicitymentioning

confidence: 90%

Section: Mycotoxins and Their Carcinogenicitymentioning

confidence: 99%

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Effects of different mycotoxins on humans, cell genome and their involvement in cancer

et al. 2017

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“…Another was that a common approach to assessing dietary intake in European countries should be elaborated. Figure 5 shows estimated dietary intake of deoxynivalenol for different population groups in several EU countries [35], compared with the tolerable dietary intake (TDI) of deoxynivalenol, as established by the JECFA [13]. Figure 5 makes clear that in some countries the TDI is exceeded for some or all intake groups of the population.…”

Section: The European Dimensionmentioning

confidence: 99%

Regulations relating to mycotoxins in food

2007

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Regulations relating to mycotoxins have been established in many countries to protect the consumer from the harmful effects of these compounds. Different factors play a role in the decision-making process of setting limits for mycotoxins. These include scientific factors, for example the availability of toxicological data and occurrence data, detailed knowledge about possibilities for sampling and analysis, and socio-economic issues. By the end of 2003, approximately 100 countries (covering approximately 85% of the world's inhabitants) had specific regulations or detailed guidelines for mycotoxins in food. The regulations were related to aflatoxins (B 1 , B 2 , G 1 and G 2 ), aflatoxin M 1 , trichothecenes (deoxynivalenol, diacetoxyscirpenol, T-2 toxin and HT-2 toxin), fumonisins (B 1 , B 2 , and B 3 ), agaric acid, ergot alkaloids, ochratoxin A, patulin, phomopsins, sterigmatocystin, and zearalenone. In Europe, and in particular in the EU, regulatory and scientific interest in mycotoxins has undergone a development in the last decade from autonomous national activity towards more EU-driven activity with a structural and network character. Harmonized EU limits now exist for 40 mycotoxin-food combinations. It is expected this number will grow in 2007 to approximately 50. The direct or indirect influence of European organizations and programs on the EU mycotoxin regulatory developments is significant. They include the European Food Safety Authority, the Scientific Cooperation on Questions relating to Food, the Rapid Alert System for Food and Feed, the creation of an EU Community Reference Laboratory for Mycotoxins and a mandate of the EC to the European Standardization Committee in methods for analysis for mycotoxins in food. Large pan-European research and networking projects as "BioCop" and "MoniQA" are also important.

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“…The recent report (Schothorst & Egmond 2004) provides the overview of Fusarium toxin levels in crops harvested in 12 European countries (Austria, Belgium, Denmark, Finland, France, Germany, Italy, the Netherlands, Norway, Portugal, Sweden, the United Kingdom). DON, NIV, T-2, and HT-25 were found in 7, 16, 20, and 14% of cereal grains examined, respectively.…”

mentioning

confidence: 99%

Occurrence of trichothecene mycotoxins in cereals harvested in the Czech Republic

Hajšlová¹,

Lancová²,

Sehnalová³

et al. 2007

Czech J. Food Sci.

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A large-scale survey of the natural occurrence of trichothecene mycotoxins in major cereals harvested in the Czech Republic was conducted during the years 1999–2001. In total, 198 cereal samples representing various wheat, barley, and rye cultivars were examined for deoxynivalenol (DON) using gas chromatography with electron capture detector (GC-ECD). Four years later, in 2005, the list of target analytes was fairly extended, 65 wheat and barley samples were analysed for seven trichothecene mycotoxins – deoxynivalenol (DON), nivalenol (NIV), fusarenon-X (Fus-X), 15-acetyldeoxynivalenol and 3-acetyldeoxynivalenol (ADONs), HT-2 toxin (HT-2). and T-2 toxin (T-2) by high performance liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). Trichothecenes represented mainly by DON were detected in almost all grain samples, its mean levels were the highest in the year 1999 which was characterised by very humid conditions during the growing season. The maximum concentration set in Commission Regulation EC (No. 856/2005) for DON (1250 µg/kg) in unprocessed cereals was exceeded only in two of all the samples analysed.

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Report from SCOOP task 3.2.10 “collection of occurrence data of Fusarium toxins in food and assessment of dietary intake by the population of EU member states”

Cited by 270 publications

References 1 publication

Effects of different mycotoxins on humans, cell genome and their involvement in cancer

Effects of different mycotoxins on humans, cell genome and their involvement in cancer

Regulations relating to mycotoxins in food

Occurrence of trichothecene mycotoxins in cereals harvested in the Czech Republic

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