Mycotoxins are secondary metabolites of fungi that are known to be associated with linear growth faltering because of their impact on inflammation, intestinal damage, inhibition of protein synthesis, and micronutrient absorption. In this narrative review, we aim to extend this analysis to further explore associations between mycotoxins (aflatoxins, ochratoxins, trichothecenes including deoxynivalenol, T-2 toxin, and fumonisins) and long-bone growth, particularly during the saltatory periods of development. Linear growth is a direct function of skeletal development and long-bone growth. We therefore explored biological pathways and mechanisms of impact of these toxins in both animal and human studies, in addition to the epidemiology literature (post-2020). Given what is known of the effects of individual and combinations of mycotoxins based on the animal literature, we have identified a need for further research and examination of how these toxins and exposures may be studied in humans to elucidate the downstream impact on bone-related biomarkers and anthropometric indices used to identify and predict stunting in population-based studies.

T-2 toxin is one of the most widespread and toxic fungal toxins in food and feed. It can cause gastrointestinal toxicity, hepatotoxicity, immunotoxicity, reproductive toxicity, neurotoxicity, and nephrotoxicity in humans and animals. T-2 toxin is physicochemically stable and does not readily degrade during food and feed processing. Therefore, suppressing T-2 toxin-induced organ toxicity through antidotes is an urgent issue. Protective agents against the organ toxicity of T-2 toxin have been recorded widely in the literature, but these protective agents and their molecular mechanisms of detoxification have not been comprehensively summarized. In this review, we provide an overview of the various protective agents to T-2 toxin and the molecular mechanisms underlying the detoxification effects. Targeting appropriate targets to antagonize T-2 toxin toxicity is also an important option. This review will provide essential guidance and strategies for the better application and development of T-2 toxin antidotes specific for organ toxicity in the future.

T-2 toxin is a representative trichothecene that is widely detected in corn, wheat and other grain feeds. T-2 toxin has stable physical and chemical properties, making it difficult to remove from food and feed. Hence, T-2 toxin has become an unavoidable pollutant in food for humans and animals. T-2 toxin can enter brain tissue by crossing the blood-brain barrier and leads to congestion, swelling and even apoptosis of neurons. T-2 toxin poisoning can directly lead to clinical symptoms (anti-feeding reaction and decline of learning and memory function in humans and animals). Maternal T-2 toxin exposure also exerted toxic effects on the central nervous system of offspring. Oxidative stress is the core neurotoxicity mechanism underlying T-2 toxin poison. Oxidative stress-mediated apoptosis, mitochondrial oxidative damage and inflammation are all involved in the neurotoxicity induced by T-2 toxin. Thus, alleviating oxidative stress has become a potential target for relieving the neurotoxicity induced by T-2 toxin. Future efforts should be devoted to revealing the neurotoxic molecular mechanism of T-2 toxin and exploring effective therapeutic drugs to alleviate T-2 toxin-induced neurotoxicity.

One of the major classes of mycotoxins posing serious hazards to humans and animals and potentially causing severe economic impact to the cereal industry are the trichothecenes, produced by many fungal genera. As such, indicative limits for the sum of T-2 and HT-2 were introduced in the European Union in 2013 and discussions are ongoing as to the establishment of maximum levels. This review provides a concise assessment of the existing understanding concerning the toxicological effects of T-2 and HT-2 in humans and animals, their biosynthetic pathways, occurrence, impact of climate change on their production and an evaluation of the analytical methods applied to their detection. This study highlights that the ecology of F. sporotrichioides and F. langsethiae as well as the influence of interacting environmental factors on their growth and activation of biosynthetic genes are still not fully understood. Predictive models of Fusarium growth and subsequent mycotoxin production would be beneficial in predicting the risk of contamination and thus aid early mitigation. With the likelihood of regulatory maximum limits being introduced, increased surveillance using rapid, on-site tests in addition to confirmatory methods will be required. allowing the industry to be proactive rather than reactive.

The presence of anorexia in animals is the most well-known clinical symptom of T-2 toxin poisoning. T-2 toxin is the most characteristic type A toxin in the trichothecene mycotoxins. The consumption of T-2 toxin can cause anorexic response in mice, rats, rabbits, and other animals. In this review, the basic information of T-2 toxin, appetite regulation mechanism and the molecular mechanism of T-2 toxin-induced anorectic response in animals are presented and discussed. The objective of this overview is to describe the research progress of anorexia in animals produced by T-2 toxin. T-2 toxin mainly causes antifeedant reaction through four pathways: vagus nerve, gastrointestinal hormone, neurotransmitter and cytokine. This review aims to give an academic basis and useable reference for the prevention and treatment of clinical symptoms of anorexia in animals resulting from T-2 toxin.

Mycotoxins can induce cell cycle disorders, cell proliferation, oxidative stress, and apoptosis through pathways such as those associated with MAPK, JAK2/STAT3, and Bcl-w/caspase-3, and cause reproductive toxicity, immunotoxicity, and genotoxicity. Previous studies have explored the toxicity mechanism of mycotoxins from the levels of DNA, RNA, and proteins, and proved that mycotoxins have epigenetic toxicity. To explore the toxic effects and mechanisms of these changes in mycotoxins, this paper summarizes the changes in DNA methylation, non-coding RNA, RNA and histone modification induced by several common mycotoxins (zearalenone, aflatoxin B1, ochratoxin A, deoxynivalenol, T-2 toxin, etc.) based on epigenetic studies. In addition, the roles of mycotoxin-induced epigenetic toxicity in germ cell maturation, embryonic development, and carcinogenesis are highlighted. In summary, this review provides theoretical support for a better understanding of the regulatory mechanism of mycotoxin epigenotoxicity and the diagnosis and treatment of diseases.

Mycotoxins are one of the most dangerous food and feed contaminants, hence they have significant influence on human and animal health. This study reviews the information reported over the last few years on the toxic effects of the most relevant and studied Fusarium toxins and their modified forms. Deoxynivalenol (DON) and its metabolites can induce intracellular oxidative stress, resulting in DNA damage. Recent studies have also revealed the capability of DON and its metabolites to disturb the cell cycle and alter amino acid expression. Several studies have attempted to explore the mechanism of action of T-2 and HT-2 toxins in anorexia induction. Among other findings, two neurotransmitters associated with this process have been identified, namely substance P and serotonin (5-hydroxytryptamine). For zearalenone (ZEN) and its metabolites, the literature points out that, in addition to their generally acknowledged estrogenic and oxidative potentials, they can also modify DNA by altering methylation patterns and histone acetylation. The ability of the compounds to induce alterations in the expression of major metabolic genes suggests that these compounds can contribute to the development of numerous metabolic diseases, including type 2 diabetes.

Mycotoxins are toxic compounds produced by fungi, which represent a risk to the food and feed supply chain, having an impact on health and economies. A high percentage of feed samples have been reported to be contaminated with more than one type of mycotoxin. Systematic, cost-effective and simple tools for testing are critical to achieve a rapid and accurate screening of food and feed quality. In this review, we describe the various aptamers that have been selected against mycotoxins and their incorporation into optical and electrochemical aptasensors, outlining the strategies exploited, highlighting the advantages and disadvantages of each approach. The review also discusses the different materials used and the immobilization methods employed, with the aim of achieving the highest sensitivity and selectivity.

T-2 toxin, an inevitable environmental pollutant, is the most toxic type A trichothecene mycotoxin. Reproductive disruption is a key adverse effect of T-2 toxin. Herein, this paper reviews the reproductive toxicity of T-2 toxin and its mechanisms in male and female members of different species. The reproductive toxicity of T-2 toxin is evidenced by decreased fertility, disrupted structures and functions of reproductive organs, and loss of gametogenesis in males and females. T-2 toxin disrupts the reproductive endocrine axis and inhibits reproductive hormone synthesis. Furthermore, exposure to T-2 toxin during pregnancy results in embryotoxicity and the abnormal development of offspring. We also summarize the research progress in counteracting the reproductive toxicity of T-2 toxin. This review provides information toward a comprehensive understanding of the reproductive toxicity mechanisms of T-2 toxin.

Due to its divergent chemical composition and good nutritional properties, pollen is not only important as a potential food supplement but also as a good substrate for the development of different microorganisms. Among such microorganisms, toxigenic fungi are extremely dangerous as they can synthesize mycotoxins as a part of their metabolic pathways. Furthermore, favorable conditions that enable the synthesis of mycotoxins (adequate temperature, relative humidity, pH, and aw values) are found frequently during pollen collection and/or production process. Internationally, several different mycotoxins have been identified in pollen samples, with a noted predominance of aflatoxins, ochratoxins, fumonisins, zearalenone, deoxynivalenol, and T-2 toxin. Mycotoxins are, generally speaking, extremely harmful for humans and other mammals. Current EU legislation contains guidelines on the permissible content of this group of compounds, but without information pertaining to the content of mycotoxins in pollen. Currently only aflatoxins have been researched and discussed in the literature in regard to proposed limits. Therefore, the aim of this review is to give information about the presence of different mycotoxins in pollen samples collected all around the world, to propose possible aflatoxin contamination pathways, and to emphasize the importance of a regular mycotoxicological analysis of pollen. Furthermore, a suggestion is made regarding the legal regulation of pollen as a food supplement and the proposed tolerable limits for other mycotoxins.