Mycotoxins defined

This same experimental approach can be used to determine the appHcabiUty of the aDAS—AP to a competitive assay for DAS. As shown in Eigure 6, increasing amounts of free DAS were used to define the 50% inhibition level (ID q) of DAS for binding of two aDAS—AP conjugates to immobilized DAS. This approach was also used to determine the sensitivity of an EIA, as well as the specificity of the assay, as shown in Table 2. Increasing amounts of trichothecene mycotoxins closely related to DAS were added to microtiter plate wells containing a constant amount of prereacted DAS—aDAS—AP. After 30 min, excess toxin and any free toxin—aDAS—AP were washed out, and substrate was added. Quantification of the color produced was directly related to the abihty of the added toxin to displace aDAS—AP from the immobilized DAS, which is an indication that the aDAS also has an avidity for that toxin. 

Tests for mycotoxin contamination can be accomplished both on the finished product and on the raw form. The latter case prevents the manufacture of an unfit product, but it often implies trouble in the evaluation of the contamination in a batch. In this case, for a defined sample size, sample preparation, and analytical method, principles are available to evaluate the accuracy of the aflatoxin determination, depending on the availability of an accurate estimate of the variability associated with each step of the analytical sequence (11,12). A valuable effort to estimate the uncertainty of the analytical sequence as a whole was carried out by the FAO (13). 

The uneven distribution of mycotoxins in grain has so far been statistically defined only for aflatoxins in a few matrices (corn, cottonseed, peanuts) (15,16), and sampling plans have been developed worldwide almost entirely for these toxins. 

Mycotoxins are defined as secondary metabolites of mould growth which are generally believed to be produced in response to stress factors acting on the fungus. Individual moulds, fungi or mycotoxins rarely occur in isolation... 

With at least two different SRM-transitions available for the analysis of a compound, one transition can be used for quantification ( quantifier ) and the other one for result confirmation ( qualifier ). If the branching ratio of quantifier to qualifier is found outside pre-defined ranges of acceptance, it is typically tried to apply a reanalysis with a more extensive chromatographic separation in order to overcome co-elution of interfering compound and analyte. This quantifier-qualifier-principle is used extensively in GC-MS and is now often applied for quantitative LC-MS/MS application too—especially in legally strictly regulated environments as forensic toxicology or pesticide and mycotoxin analysis in feed and foodstuff [55], In contrast,... 

The regulatory issues are less well-defined for mycotoxins other than aflatoxins. But with increasing data on specific toxicity of Fusarium mycotoxins such as fiimonisins, regulatory guidelines are being considered for these toxins as well. For example, in the USA, advisory limits exist for deoxynivalenol (DON) at 5-lOmg/kg (5-10 parts per million ppm) in animal feeds [7]. 

Mycotoxins are defined as mould derived secondary metabohtes and include Ochratoxin A (OTA). OTA, produced by Aspergillus ochraeus and Penicillium ver-rucosum, can be found as a contaminant in grain, beer, coffee and meat. OTA is nephrotoxic, hepatotoxic and carcinogenic [197]. 

Mycotoxins are secondary metabolites of molds (primarily deuteromycetes), which are generally produced under optimum conditions at the end of the exponential growth phase. The term mycotoxin combines the terms mykes, the Greek word for molds, and toxicum, the Latin word for toxic or poisonous. Accordingly, mycotoxins occasionally also are defined as... 

Summary Primary hepatocellular carcinoma is one of the most common cancers in the world and is prevalent on the continents of Africa and Asia. A number of classical epidemiological studies have determined that the exposure status of people to aflatoxin B1 is an important risk factor in the etiology of liver cancer. However, these studies have only relied upon the criteria of presumptive intake data, rather than information obtained from quantitative analyses of food samples, biological fluids and from people exposed to aflatoxin. Information obtained by monitoring exposed individuals for specific DNA adducts and metabolites will define the pharmacokinetics of aflatoxin B1 in people, thereby facilitating risk assessments. Preliminary data, reported here, support the concept that measurement of the major, rapidly excised AFB-N7-Gua adduct in urine and quantification of the more persistent aflatoxin albumin adduct are appropriate dosimeters for estimating exposure status and possibly risk in individuals consuming this mycotoxin. 

Among all mycotoxins, aflatoxins are the most toxic, widespread, and the strongest natural carcinogens (Table 11.2). The International Agency for Research on Cancer (lARC) has defined aflatoxin B1 (AFBl) as a carcinogen [11]. 

However narrowly they are defined, the mycotoxins do not constitute a chemical category and they have no molecular features in common. All that... 

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