Nrf2: A Main Responsive Element of the Toxicity Effect Caused by Trichothecene (T-2) Mycotoxin.
Youshuang WangYu LiuTingyu HuangYunhe ChenWenxi SongFengjuan ChenYibao JiangCong ZhangXu YangPublished in: Toxics (2023)
T-2 toxin, the most toxic type A trichothecene mycotoxin, is produced by Fusarium, and is widely found in contaminated feed and stored grains. T-2 toxin is physicochemically stable and is challenging to eradicate from contaminated feed and cereal, resulting in food contamination that is inescapable and poses a major hazard to both human and animal health, according to the World Health Organization. Oxidative stress is the upstream cause of all pathogenic variables, and is the primary mechanism through which T-2 toxin causes poisoning. Nuclear factor E2-related factor 2 (Nrf2) also plays a crucial part in oxidative stress, iron metabolism and mitochondrial homeostasis. The major ideas and emerging trends in future study are comprehensively discussed in this review, along with research progress and the molecular mechanism of Nrf2's involvement in the toxicity impact brought on by T-2 toxin. This paper could provide a theoretical foundation for elucidating how Nrf2 reduces oxidative damage caused by T-2 toxin, and a theoretical reference for exploring target drugs to alleviate T-2 toxin toxicity with Nrf2 molecules.
Keyphrases
- oxidative stress
- escherichia coli
- nuclear factor
- diabetic rats
- ischemia reperfusion injury
- dna damage
- induced apoptosis
- drinking water
- toll like receptor
- healthcare
- public health
- heavy metals
- risk assessment
- endothelial cells
- immune response
- room temperature
- ionic liquid
- endoplasmic reticulum stress
- health information
- climate change