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Review
. 2020 Jan 9;10:2908.
doi: 10.3389/fmicb.2019.02908. eCollection 2019.

Toxicological and Medical Aspects of Aspergillus-Derived Mycotoxins Entering the Feed and Food Chain

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Free PMC article
Review

Toxicological and Medical Aspects of Aspergillus-Derived Mycotoxins Entering the Feed and Food Chain

Zsolt Ráduly et al. Front Microbiol. .
Free PMC article

Abstract

Due to Earth's changing climate, the ongoing and foreseeable spreading of mycotoxigenic Aspergillus species has increased the possibility of mycotoxin contamination in the feed and food production chain. These harmful mycotoxins have aroused serious health and economic problems since their first appearance. The most potent Aspergillus-derived mycotoxins include aflatoxins, ochratoxins, gliotoxin, fumonisins, sterigmatocystin, and patulin. Some of them can be found in dairy products, mainly in milk and cheese, as well as in fresh and especially in dried fruits and vegetables, in nut products, typically in groundnuts, in oil seeds, in coffee beans, in different grain products, like rice, wheat, barley, rye, and frequently in maize and, furthermore, even in the liver of livestock fed by mycotoxin-contaminated forage. Though the mycotoxins present in the feed and food chain are well documented, the human physiological effects of mycotoxin exposure are not yet fully understood. It is known that mycotoxins have nephrotoxic, genotoxic, teratogenic, carcinogenic, and cytotoxic properties and, as a consequence, these toxins may cause liver carcinomas, renal dysfunctions, and also immunosuppressed states. The deleterious physiological effects of mycotoxins on humans are still a first-priority question. In food production and also in the case of acute and chronic poisoning, there are possibilities to set suitable food safety measures into operation to minimize the effects of mycotoxin contaminations. On the other hand, preventive actions are always better, due to the multivariate nature of mycotoxin exposures. In this review, the occurrence and toxicological features of major Aspergillus-derived mycotoxins are summarized and, furthermore, the possibilities of treatments in the medical practice to heal the deleterious consequences of acute and/or chronic exposures are presented.

Keywords: aflatoxins; carcinogenic; food poisoning; fumonisins; mycotoxin; ochratoxins; secondary metabolites; sterigmatocystin.

Figures

FIGURE 1
FIGURE 1
The risk of mycotoxin exposure. Milestones in mycotoxicology: (1) In 1962, mycotoxins are identified as cause of turkey “X” disease; (2) Aflatoxin outbreak in Gambia in 1988, No. subjects: 391; (3) Aflatoxin poisoning in Egypt in 1992, No. subjects: 19; (4) Aflatoxin outbreak in Guinea in 1999, No. subjects: approx. 600; and (5) Aflatoxin outbreak in Kenya 2004, No. subjects: approx. 100; (a) Due to the climate change and increasing mean temperature, mycotoxin-producing fungi spread to the north. (b) Monoculture farming is sensitive to mold infestation. (c) Strict federal regulation can prevent the spread of mold. (d) The strict regulation of import and export are important to minimalize mycotoxin contaminations. (e) Prevention of mycotoxin infestation is of primary importance. Without sufficient education and up-to-date methods, it is hard to store, process, transport, or even analyze properly and safely food and feed. (f) Mycotoxins have serious economic and financial consequences (see references in the text).
FIGURE 2
FIGURE 2
Chemical structure of some carcinogenic aflatoxins.
FIGURE 3
FIGURE 3
Chemical structures of ochratoxin A, patulin, gliotoxin, and fumonisins.
FIGURE 4
FIGURE 4
Toxicological effects of mycotoxins in the human body. Fumonisins can alter the sphingolipid metabolism, and it has an effect on the membrane of different cells like neurons. Fumonisins may increase the possibility of esophageal cancer formation. With different molecular pathways, aflatoxin, gliotoxin, fumonisin, and patulin can suppress several immunological mechanisms. Aflatoxins affect the pairing of nucleotides. Mutations of proto-oncogenes or tumor suppressor genes can cause liver cancer. Aflatoxin metabolites produced by the hepatic CYP enzymes can lead to chromosomal DNA strand breaks. Aflatoxins can inhibit cell proliferation. In the gut, mycotoxins can interfere with the regeneration of the gastrointestinal tract forming cells. Gliotoxin can penetrate the blood–brain barrier, and due to its cytotoxicity, it can damage the astrocytes. Sterigmatocystin may cause esophageal cancer. Ochratoxin A is nephrotoxic and can cause kidney damage, cancer, or renal failure. OTA was recently connected to Balkan Endemic Nephropathy (BEN) kidney disease and chronic interstitial nephropathy (for references, see the text).
FIGURE 5
FIGURE 5
Countries of origin for aflatoxin-related notifications in food based on the European Union (EU) Rapid Alert System for Food and Feed (RASFF) database from 1st January 2009 until 27th June 2019 (European Parliament and of the Council, 2002).
FIGURE 6
FIGURE 6
Risk of mycotoxin exposure in the feed and food chain. Mycotoxins, like aflatoxins (e.g., AFB1), go through biotransformation in the livestock and different metabolites are produced, such as AFM1, which can be excreted into the milk, where AFM1 can bind to casein. After digestion, AFM1 is released from the casein – AFM1 complexes. The consumption of high amounts of dairy products contaminated with AFM1 can lead to acute mycotoxicosis (for references, see the text). The carry-over rates of mycotoxins show seasonal differences, and there are other diverse factors influencing the prevalence of carry-over, e.g., the quantity of mycotoxins in the feed and the excreted amount of toxin in the milk. The geographical location and feeding practice could also affect the carry-over rates, which could be even 6%, regarding AFs (Völkel et al., 2011).
FIGURE 7
FIGURE 7
The severity of consequences of mycotoxins in the different stages of life.
FIGURE 8
FIGURE 8
Possible target points for therapy.

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