Antioxidant agents against trichothecenes: new hints for oxidative stress treatment

Abstract

Trichothecenes are a group of mycotoxins mainly produced by fungi of genus Fusarium. Due to high toxicity and widespread dissemination, T-2 toxin and deoxynivalenol (DON) are considered to be the most important compounds of this class. Trichothecenes generate free radicals, including reactive oxygen species (ROS), which induce lipid peroxidation, decrease levels of antioxidant enzymes, and ultimately lead to apoptosis. Consequently, oxidative stress is an active area of research on the toxic mechanisms of trichothecenes, and identification of antioxidant agents that could be used against trichothecenes is crucial for human health. Numerous natural compounds have been analyzed and have shown to function very effectively as antioxidants against trichothecenes. In this review, we summarize the molecular mechanisms underlying oxidative stress induced by these compounds, and discuss current knowledge regarding such antioxidant agents as vitamins, quercetin, selenium, glucomannan, nucleotides, antimicrobial peptides, bacteria, polyunsaturated fatty acids, oligosaccharides, and plant extracts. These products inhibit trichothecene-induced oxidative stress by (1) inhibiting ROS generation and induced DNA damage and lipid peroxidation; (2) increasing antioxidant enzyme activity; (3) blocking the MAPK and NF-κB signaling pathways; (4) inhibiting caspase activity and apoptosis; (5) protecting mitochondria; and (6) regulating anti-inflammatory actions. Finally, we summarize some decontamination methods, including bacterial and yeast biotransformation and degradation, as well as mycotoxin-binding agents. This review provides a comprehensive overview of antioxidant agents against trichothecenes and casts new light on the attenuation of oxidative stress.

JNK signaling in cancer cell survival

“…Studies in Jnk knockout mice revealed that JNK1 promotes the survival of activated T cells during immune responses and that JNK2 modulates CD8 + T cell expansion . Our group recently showed that JNK1/STAT3 is a prosurvival hub that inhibits RAW264.7 cell apoptosis . The JNK1/STAT3 pathway can maintain the normal function of mitochondria and to inhibit T‐2 toxin‐induced cell apoptosis …”

“…68 Our group recently showed that JNK1/STAT3 is a prosurvival hub that inhibits RAW264.7 cell apoptosis. 43,69,70 The JNK1/ STAT3 pathway can maintain the normal function of mitochondria and to inhibit T-2 toxin-induced cell apoptosis. 43 JNK1 and JNK2 regulate the expression of the central transcription initiation factor TATA-binding protein (TBP).…”

“…Autophagy promotes cell and organism survival in various contexts, including endoplasmic reticulum (ER) stress, ontological development, microbial infection, and diseases that are characterized by the accumulation of protein aggregates. 69,70,99 JNK positively regulates autophagy and contributes to cell survival. 46 Ogata et al 100 showed that JNK-mediated autophagy activation is essential for SK-N-SH neuroblastoma cell survival after ER stress.…”

Protective Role of Hydrogen Gas on Oxidative Damage and Apoptosis in Intestinal Porcine Epithelial Cells (IPEC-J2) Induced by Deoxynivalenol: A Preliminary Study

“…Trichothecenes generate free radicals, reduce antioxidant enzymes activities, and ultimately induce apoptosis in cells [37]. A previous report indicated that 10 µM DON had toxic effects on IPEC-J2 cells, which caused cell rounding, autolysis, and detachment from the monolayer, also increasing LDH release into the medium [26].…”

“…It was shown that trichothecene mycotoxins can induce cellular oxidative stress, such as accumulation of ROS, increasing lipid peroxidation, and affecting the antioxidant system [37]. Among ROS, •OH and ONOO − are cytotoxic to cells and rapidly induce cell damage; however, they are exceedingly unsteady in living cells because of a short biological half-life caused by their strong oxidative capabilities [38].…”