Prevalent Mycotoxins in Animal Feed: Occurrence and Analytical Methods.

Today, we have been witnessing a steady tendency in the increase of global demand for maize, wheat, soybeans, and their products due to the steady growth and strengthening of the livestock industry. Thus, animal feed safety has gradually become more important, with mycotoxins representing one of the most significant hazards. Mycotoxins comprise different classes of secondary metabolites of molds. With regard to animal feed, aflatoxins, fumonisins, ochratoxins, trichothecenes, and zearalenone are the more prevalent ones. In this review, several constraints posed by these contaminants at economical and commercial levels will be discussed, along with the legislation established in the European Union to restrict mycotoxins levels in animal feed. In addition, the occurrence of legislated mycotoxins in raw materials and their by-products for the feeds of interest, as well as in the feeds, will be reviewed. Finally, an overview of the different sample pretreatment and detection techniques reported for mycotoxin analysis will be presented, the main weaknesses of current methods will be highlighted.

Controversies in fumonisin mycotoxicology and risk assessment.

Fusarium verticillioides causes several animal diseases and the contamination maize suggests that it could adversely affect human health. The fumonisin B mycotoxins were characterized from the fungal culture material and shown to be the causative principle responsible for the major mycotoxicological effects of the fungus in experimental and farm animals. The main focus was on the toxicological effects in rats and mice, the outcome of which played an important role in setting risk assessment parameters for exposure of the fumonisins to humans. The International Agency for Research on Cancer characterized the fumonisins as Group 2B carcinogens. Several controversial findings regarding the toxicological effects of the culture material of the fungus, the genotoxicity and carcinogenicity of pure fumonisin B(1) (FB(1)) in rats have been reported that should be clarified prior to assessing the risk in humans. The underlying differences between the diets with the high protein levels are likely to sensitize the kidneys to FB(1)-induced toxic and carcinogenic effects. Several other dietary factors, such as plant extracts (antioxidants) and dietary Fe, could either stimulate or inhibit cancer induction of FB(1), which complicates the comparison of toxicological effects in experimental animals. Cognisance should be taken of the modulating role of dietary constituents as it will determine the outcome of toxicological assays and determine the threshold of an adverse effect in a specific target organ to be used in determining risk assessment parameters.

Development and validation of a method based on a QuEChERS procedure and heart-cutting GC-MS for determination of five mycotoxins in cereal products.

A new analytical method for the rapid and simultaneous determination of five mycotoxins (zearelenone, deoxynivalenol, Fusarenon X, 15-acetyldeoxynivalenol and nivalenol) in breakfast cereals and flours by heart-cutting GC-MS has been developed and validated. Extraction was performed with MeCN, applying a modified QuEChERS (QUick, Easy, CHeap, Effective, Rugged and Safe) procedure, and the extracts were analyzed after a silylation of the analytes under study. Careful optimization of the parameters of Deans Switch device and GC-MS was achieved in order to attain a fast separation in SIM mode, allowing a total run time of only 8 min. Acceptable recoveries for all mycotoxins at two different spiking levels (20 and 100 microg/kg) were achieved with good repeatability (from 9 to 21%). LOD ranged from 2 to 15 microg/kg and LOQ ranged from 5 to 50 microg/kg, which were lower than the maximum limit legal established by the European Union (EU). The method developed was applied to commercial breakfast cereals and flours; among the mycotoxins studied, deoxynivalenol and zearalenone were the most predominant.

Evolving global epidemiology, syndromic classification, general management, and prevention of unknown mushroom poisonings.

OBJECTIVE: To assess the evolving global epidemiology of mushroom poisoning and to identify new and emerging mushroom poisonings and their treatments, a descriptive analysis and review of the world's salient scientific literature on mushroom poisoning was conducted. DATA SOURCE: Data sources from observation studies conducted over the period 1959-2002 and describing 28,018 mushroom poisonings since 1951 were collected from case reports, case series, regional descriptive studies, meta-analyses, and laboratory studies of mushroom poisonings and the toxicokinetics of mycotoxins. STUDY SELECTION: Studies included in the review were selected by a MEDLINE search, 1966-2004, an Ovid OLDMEDLINE search, 1951-1965, and a medical library search for sources published before 1951. DATA EXTRACTION: To better guide clinicians in establishing diagnoses and implementing therapies, despite confusing ingestion histories, data were extracted to permit an expanded syndromic classification of mushroom poisoning based on presentation timing and target organ systemic toxicity. DATA SYNTHESIS: The final 14 major syndromes of mushroom poisoning were stratified first by presentation timing and then by target organ systemic toxicity and included early (<6 hrs), late (6-24 hrs), and delayed syndromes (> or =1 day). There were eight early syndromes (four neurotoxic, two gastrointestinal, two allergic); three late syndromes (hepatotoxic, accelerated nephrotoxic, erythromelalgia); and three delayed syndromes (delayed nephrotoxic, delayed neurotoxic, rhabdomyolysis). Four new mushroom poisoning syndromes were classified including accelerated nephrotoxicity (Amanita proxima, Amanita smithiana), rhabdomyolysis (Tricholoma equestre, Russula subnigricans), erythromelalgia (Clitocybe amoenolens, Clitocybe acromelalgia), and delayed neurotoxicity (Hapalopilus rutilans). In addition, data sources were stratified by three chronological time periods with >1,000 confirmed mushroom ingestions reported and tested for any statistically significant secular trends in case fatalities from mushroom ingestions over the entire study period, 1951-2002. CONCLUSIONS: Since the 1950s, reports of severe and fatal mushroom poisonings have increased worldwide. Clinicians must consider mushroom poisoning in the evaluation of all patients who may be intoxicated by natural substances. Since information on natural exposures is often insufficient and incorrect, a new syndromic classification of mushroom poisoning is recommended to guide clinicians in making earlier diagnoses, especially in cases where only advanced critical care, including organ transplantation, may be life saving.

Implications of apoptosis for toxicity, carcinogenicity, and risk assessment: fumonisin B(1) as an example.

The rates of cell proliferation and cell loss in conjunction with the differentiation status of a tissue are among the many factors contributing to carcinogenesis. Nongenotoxic (non-DNA reactive) chemicals may affect this balance by increasing proliferation through direct mitogenesis or through a regenerative response following loss of cells through cytotoxic (oncotic) or apoptotic necrosis. In a recent NTP study in Fischer rats and B6C3F(1) mice, the mycotoxin fumonisin B(1) caused renal carcinomas in male rats and liver cancer in female mice. In an earlier study in male BD-IX rats, fumonisin B(1) caused hepatic toxicity and hepatocellular carcinomas. An early effect of fumonisin B(1) exposure in these target organs is apoptosis. However, there is also some evidence of oncotic necrosis following fumonisin B(1) administration, especially in the liver. Induction of apoptosis may be a consequence of ceramide synthase inhibition and disruption of sphingolipid metabolism by fumonisin B(1). Fumonisin B(1) is not genotoxic in bacterial mutagenesis screens or in the rat liver unscheduled DNA-synthesis assay. Fumonisin B(1) may be the first example of an apparently nongenotoxic (non-DNA reactive) agent producing tumors through a mode of action involving apoptotic necrosis, atrophy, and consequent regeneration.

Deterioro fúngico de los alimentos e impactos económicos de las micotoxinas / Fungal biodeterioration of food and economic impact of mycotoxins

Las micotoxinas son metabólitos fúngicos que se encuentran en una variedad de sustratos incluyendo piensos y alimentos. Ellos causan problemas en la salud humana y animal especialmente, causan pérdidas económicas significativas. La toxicidad de las micotoxinas en los animales varía desde muerte aguda a enfermedades crónicas e interferencia con la eficiencia reproductiva. Las aflatoxinas causan daño del hígado, cáncer, disminución de la producción de leche, huevos e inmunosupresión. Las aflotoxinas son de gran importancia en las micotoxicosis en humanos ya que son potencialmente carcinogénicas. Los principales estudios epidemiológicos relacionados con las afloxinas han sido llevados a cabo en Asia y africa, y algunos han mostrado una asociación positiva entre niveles de aflatoxinas en los alimentos y presencia de enfermedades. Las pérdidas económicas debido a las micotoxinas y en especial a aflatoxinas son multifacéticas e involucra al cultivo directamente y animales domésticos. La incidencia de las micotoxinas varía entre sustratos, condiciones climáticas y regiones. Por estas razones, la importancia económica de las micotoxinas es difícil de cuantificar