T-2 mycotoxin: toxicological effects and decontamination strategies

Abstract

Mycotoxins are highly diverse secondary metabolites produced in nature by a wide variety of fungus which causes food contamination, resulting in mycotoxicosis in animals and humans. In particular, trichothecenes mycotoxin produced by genus fusarium is agriculturally more important worldwide due to the potential health hazards they pose. It is mainly metabolized and eliminated after ingestion, yielding more than 20 metabolites with the hydroxy trichothecenes-2 toxin being the major metabolite. Trichothecene is hazardously intoxicating due to their additional potential to be topically absorbed, and their metabolites affect the gastrointestinal tract, skin, kidney, liver, and immune and hematopoietic progenitor cellular systems. Sensitivity to this type of toxin varying from dairy cattle to pigs, with the most sensitive endpoints being neural, reproductive, immunological and hematological effects. The mechanism of action mainly consists of the inhibition of protein synthesis and oxidative damage to cells followed by the disruption of nucleic acid synthesis and ensuing apoptosis. In this review, the possible hazards, historical significance, toxicokinetics, and the genotoxic and cytotoxic effects along with regulatory guidelines and recommendations pertaining to the trichothecene mycotoxin are discussed. Furthermore, various techniques utilized for toxin determination, pathophysiology, prophylaxis and treatment using herbal antioxidant compounds and regulatory guidelines and recommendations are reviewed. The prospects of the trichothecene as potential hazardous agents, decontamination strategies and future perspectives along with plausible therapeutic uses are comprehensively described.

Keywords: apoptosis; decontamination; herbal antioxidant compounds; oxidative damage; trichothecenes.

Figure 1. Schematic representation of T-2 toxin by its toxic and safe design

Figure 2. Structures of T-2 and HT-2 toxins (type A) and other trichothecenes (types B, C, and D)

Figure 3. Microbial transformation of trichothecenes into their de-epoxylated forms

Figure 4. Diagrammatic representation of altered metabolic pathways in different organs of Wistar rats followed by T-2 toxin treatment

Metabolites shown in red or blue denote a significant increase or decrease in T-2 toxin treated rats with respect to control rats. Metabolites shown in black denote no marked change. (Reproduced from Wan Q et al. 2015 Mol. Biosyst. with permission of The Royal Society of Chemistry).

Figure 5. The impact of T-2 mycotoxins on the human intestinal gut region against infection by salmonella

(Reproduced from Antonissen et al., 2014, with the permission of the Toxin Journal).

Figure 6. Role of the T-2 toxin in causing ROS-mediated caspase-dependent and independent apoptosis in human cells

Figure 7. Three targeting strategies in a T-2-toxin-based therapy

(Reproduced from Shapira A 2010 with the permission of the Toxin Journal).