Modified Fusarium mycotoxins unmasked: From occurrence in cereals to animal and human excretion

With an average annual production of 6.9 M tonnes and 2.5 M tonnes of maize and wheat respectively, Serbia is one of the main grain producers and exporters in Europe. Cereals are also the major staple food in Serbian diet. In view of the high cereal consumption, for human and animal nutrition, the presence of mycotoxins entails a high public health risk of chronic exposure to mycotoxins. This study provides an overview of the incidence of predominant mycotoxins, mainly in cereal and dairy products, in Serbia, in the 2004–2016, using data reported in the scientific literature. The study demonstrated that the total prevalence of aflatoxins was 62.9% (n = 12,517) with 26.2% of the samples exceeding the EU limits during this period. Results obtained for T-2/HT-2 (n = 523), deoxynivalenol (n = 2907), fumonisins (n = 998), zearalenone (n = 689) and ochratoxin A (n = 740) indicated the prevalence of 45.5%, 42.9%, 63.3%, 39.3% and 28.1%, respectively. For these mycotoxins, the EU limits were less frequently exceeded. Comprehensive collection and analysis of all accessible information reviewed in this paper showed moderate incidence and prevalence of mycotoxins in Serbia, with an exception of the 2012 drought year and the 2014 flood year.

Section: Introductionmentioning

confidence: 99%

Overview on the Mycotoxins Incidence in Serbia in the Period 2004–2016

Udovički

Audenaert

Saeger

et al. 2018

“…Modification of mycotoxins may be triggered by food processing, or matrix related, or through conjugation by either plant, fungi or animal [16,17]. These modified mycotoxins often escape routine analysis leading to underestimation of actual mycotoxin levels in products and may possibly hydrolysed into the parent toxins during digestion [18]. Several studies on the occurrence of Fusarium mycotoxins in cereals and cereal-based products have reported the natural occurrence and co-occurrence of modified mycotoxins such as DON-3-glucoside (DON-3G), ZEN-4-glucoside (ZEN-14G), and α- and β-zearalenol-4-glucoside (α- and β-ZEL-4G) [5,19].…”

Section: Introductionmentioning

confidence: 99%

Occurrence of Fusarium Mycotoxins in Cereal Crops and Processed Products (Ogi) from Nigeria

Chilaka

Boevre

Atanda

et al. 2016

In Nigeria, maize, sorghum, and millet are very important cash crops. They are consumed on a daily basis in different processed forms in diverse cultural backgrounds. These crops are prone to fungi infestation, and subsequently may be contaminated with mycotoxins. A total of 363 samples comprising of maize (136), sorghum (110), millet (87), and ogi (30) were collected from randomly selected markets in four agro-ecological zones in Nigeria. Samples were assessed for Fusarium mycotoxins contamination using a multi-mycotoxin liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. Subsequently, some selected samples were analysed for the occurrence of hidden fumonisins. Overall, 64% of the samples were contaminated with at least one toxin, at the rate of 77%, 44%, 59%, and 97% for maize, sorghum, millet, and ogi, respectively. Fumonisins were the most dominant, especially in maize and ogi, occurring at the rate of 65% and 93% with mean values of 935 and 1128 μg/kg, respectively. The prevalence of diacetoxyscirpenol was observed in maize (13%), sorghum (18%), and millet (29%), irrespective of the agro-ecological zone. Other mycotoxins detected were deoxynivalenol, zearalenone, and their metabolites, nivalenol, fusarenon-X, HT-2 toxin, and hidden fumonisins. About 43% of the samples were contaminated with more than one toxin. This study suggests that consumption of cereals and cereal-based products, ogi particularly by infants may be a source of exposure to Fusarium mycotoxins.

“…In addition to native/unmodified mycotoxins, food and feeds also contain mycotoxin derivatives that may represent a risk for animals and humans, their metabolic fate and toxicity being not always characterized [4,17,18,19]. Although new molecules are regularly described, the major derivatives of DON present in food and feed correspond to fungal (i.e., the acetylated derivatives: 3- and 15-acetylDON or 3ADON and 15ADON) and plant (i.e., 3- O -glucoside-DON or D3G) derivatives [17,19].…”

Section: Introductionmentioning

confidence: 99%

“…Although new molecules are regularly described, the major derivatives of DON present in food and feed correspond to fungal (i.e., the acetylated derivatives: 3- and 15-acetylDON or 3ADON and 15ADON) and plant (i.e., 3- O -glucoside-DON or D3G) derivatives [17,19]. 3/15ADON (Figure 1) are precursors in the synthesis of DON [20] and are thus found in food as a mixture with DON.…”

Section: Introductionmentioning

confidence: 99%

Hydrolytic Fate of 3/15-Acetyldeoxynivalenol in Humans: Specific Deacetylation by the Small Intestine and Liver Revealed Using in Vitro and ex Vivo Approaches

Ajandouz

Berdah

Moutardier

et al. 2016

In addition to deoxynivalenol (DON), acetylated derivatives, i.e., 3-acetyl and 15-acetyldexynivalenol (or 3/15ADON), are present in cereals leading to exposure to these mycotoxins. Animal and human studies suggest that 3/15ADON are converted into DON after their ingestion through hydrolysis of the acetyl moiety, the site(s) of such deacetylation being still uncharacterized. We used in vitro and ex vivo approaches to study the deacetylation of 3/15ADON by enzymes and cells/tissues present on their way from the food matrix to the blood in humans. We found that luminal deacetylation by digestive enzymes and bacteria is limited. Using human cells, tissues and S9 fractions, we were able to demonstrate that small intestine and liver possess strong deacetylation capacity compared to colon and kidneys. Interestingly, in most cases, deacetylation was more efficient for 3ADON than 15ADON. Although we initially thought that carboxylesterases (CES) could be responsible for the deacetylation of 3/15ADON, the use of pure human CES1/2 and of CES inhibitor demonstrated that CES are not involved. Taken together, our original model system allowed us to identify the small intestine and the liver as the main site of deacetylation of ingested 3/15ADON in humans.