Pathological consequences, metabolism and toxic effects of trichothecene T-2 toxin in poultry

Abstract

Contamination of feed with mycotoxins has become a severe issue worldwide. Among the most prevalent trichothecene mycotoxins, T-2 toxin is of particular importance for livestock production, including poultry posing a significant threat to animal health and productivity. This review article aims to comprehensively analyze the pathological consequences, metabolism, and toxic effects of T-2 toxin in poultry. Trichothecene mycotoxins, primarily produced by Fusarium species, are notorious for their potent toxicity. T-2 toxin exhibits a broad spectrum of negative effects on poultry species, leading to substantial economic losses as well as concerns about animal welfare and food safety in modern agriculture. T-2 toxin exposure easily results in negative pathological consequences in the gastrointestinal tract, as well as in parenchymal tissues like the liver (as the key organ for its metabolism), kidneys, or reproductive organs. In addition, it also intensely damages immune system-related tissues such as the spleen, the bursa of Fabricius, or the thymus causing immunosuppression and increasing the susceptibility of the animals to infectious diseases, as well as making immunization programs less effective. The toxin also damages cellular processes on the transcriptional and translational levels and induces apoptosis through the activation of numerous cellular signaling cascades. Furthermore, according to recent studies, besides the direct effects on the abovementioned processes, T-2 toxin induces the production of reactive molecules and free radicals resulting in oxidative distress and concomitantly occurring cellular damage. In conclusion, this review article provides a complex and detailed overview of the metabolism, pathological consequences, mechanism of action as well as the immunomodulatory and oxidative stress-related effects of T-2 toxin. Understanding these effects in poultry is crucial for developing strategies to mitigate the impact of the T-2 toxin on avian health and food safety in the future.