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Nrf2:单端孢霉烯族毒素(T-2)霉菌毒素所致毒性效应的主要反应元件

Nrf2: A Main Responsive Element of the Toxicity Effect Caused by Trichothecene (T-2) Mycotoxin.

作者信息

Wang Youshuang, Liu Yu, Huang Tingyu, Chen Yunhe, Song Wenxi, Chen Fengjuan, Jiang Yibao, Zhang Cong, Yang Xu

机构信息

College of Veterinary Medicine, Henan Agricultural University, No. 15 Longzihu University Park, Zhengdong New District, Zhengzhou 450002, China.

College of Animal Science and Technology, Henan Agricultural University, Zhengzhou 450002, China.

出版信息

Toxics. 2023 Apr 21;11(4):393. doi: 10.3390/toxics11040393.


DOI:10.3390/toxics11040393
PMID:37112621
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10146852/
Abstract

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.

摘要

T-2毒素是毒性最强的A型单端孢霉烯族霉菌毒素,由镰刀菌产生,广泛存在于受污染的饲料和储存谷物中。T-2毒素在物理化学性质上很稳定,要从受污染的饲料和谷物中根除具有挑战性,导致食物污染难以避免,对人类和动物健康都构成重大危害,世界卫生组织如是说。氧化应激是所有致病变量的上游原因,是T-2毒素导致中毒的主要机制。核因子E2相关因子2(Nrf2)在氧化应激、铁代谢和线粒体稳态中也起着关键作用。本综述全面讨论了未来研究的主要观点和新趋势,以及Nrf2参与T-2毒素所致毒性影响的研究进展和分子机制。本文可为阐明Nrf2如何减轻T-2毒素引起的氧化损伤提供理论基础,也可为探索以Nrf2分子减轻T-2毒素毒性的靶向药物提供理论参考。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/f43bd708f336/toxics-11-00393-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/0c2e276e19f5/toxics-11-00393-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/28e8cd06411b/toxics-11-00393-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/553023761c34/toxics-11-00393-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/b64282ff2530/toxics-11-00393-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/2dee8f8e10f6/toxics-11-00393-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/98a200e2afee/toxics-11-00393-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/01275e357c44/toxics-11-00393-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/f43bd708f336/toxics-11-00393-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/0c2e276e19f5/toxics-11-00393-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/28e8cd06411b/toxics-11-00393-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/553023761c34/toxics-11-00393-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/b64282ff2530/toxics-11-00393-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/2dee8f8e10f6/toxics-11-00393-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/98a200e2afee/toxics-11-00393-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/01275e357c44/toxics-11-00393-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b99/10146852/f43bd708f336/toxics-11-00393-g008.jpg

相似文献

[1]
Nrf2: A Main Responsive Element of the Toxicity Effect Caused by Trichothecene (T-2) Mycotoxin.

Toxics. 2023-4-21

[2]
NRF2/PGC-1α-mediated mitochondrial biogenesis contributes to T-2 toxin-induced toxicity in human neuroblastoma SH-SY5Y cells.

Toxicol Appl Pharmacol. 2022-9-15

[3]
T-2 Toxin-The Most Toxic Trichothecene Mycotoxin: Metabolism, Toxicity, and Decontamination Strategies.

Molecules. 2021-11-14

[4]
Pathological consequences, metabolism and toxic effects of trichothecene T-2 toxin in poultry.

Poult Sci. 2024-3

[5]
T-2 toxin metabolism and its hepatotoxicity: New insights on the molecular mechanism and detoxification.

Environ Pollut. 2023-8-1

[6]
Fusarial toxins: secondary metabolites of Fusarium fungi.

Rev Environ Contam Toxicol. 2014

[7]
Overview of T-2 Toxin Enterotoxicity: From Toxic Mechanisms and Detoxification to Future Perspectives.

J Agric Food Chem. 2024-2-21

[8]
An in-depth review of the dermal toxicity of T-2 toxin: Clinical symptoms, injury mechanisms, and treatment approach.

Food Chem Toxicol. 2024-11

[9]
T-2 toxin neurotoxicity: role of oxidative stress and mitochondrial dysfunction.

Arch Toxicol. 2019-9-30

[10]
Review of neurotoxicity of T-2 toxin.

Mycotoxin Res. 2024-2

引用本文的文献

[1]
T-2 Toxin-Induced Hepatotoxicity in HepG2 Cells Involves the Inflammatory and Nrf2/HO-1 Pathways.

Toxins (Basel). 2025-8-8

[2]
Environmental Toxins and Oxidative Stress: The Link to Cardiovascular Diseases.

Antioxidants (Basel). 2025-5-17

[3]
Peroxiredoxin 4 Ameliorates T-2 Toxin-Induced Growth Retardation in GH3 Cells by Inhibiting Oxidative Stress and Apoptosis.

Molecules. 2024-11-21

本文引用的文献

[1]
Ameliorates Neural Damage Induced by Experimental Ischemic Stroke and Radiation Exposure.

Front Biosci (Landmark Ed). 2023-2-24

[2]
Possible Mechanisms of Oxidative Stress-Induced Skin Cellular Senescence, Inflammation, and Cancer and the Therapeutic Potential of Plant Polyphenols.

Int J Mol Sci. 2023-2-13

[3]
Direct interaction between mortalin and HIF-1α at the mitochondria inhibits apoptosis by blocking recruitment of Bax.

FEBS J. 2023-8

[4]
Calycosin-7-glucoside promotes mitochondria-mediated apoptosis in hepatocellular carcinoma by targeting thioredoxin 1 to regulate oxidative stress.

Chem Biol Interact. 2023-4-1

[5]
Nrf2/PINK1-mediated mitophagy induction alleviates sodium fluoride-induced hepatic injury by improving mitochondrial function, oxidative stress, and inflammation.

Ecotoxicol Environ Saf. 2023-3-1

[6]
Current understanding of the immune potential of B-cell subsets in malarial pathogenesis.

Front Microbiol. 2023-1-26

[7]
Water extract from Herpetospermum pedunculosum attenuates oxidative stress and ferroptosis induced by acetaminophen via regulating Nrf2 and NF-κB pathways.

J Ethnopharmacol. 2023-4-6

[8]
The role of cholesterol and mitochondrial bioenergetics in activation of the inflammasome in IBD.

Front Immunol. 2022

[9]
MiR-140 is involved in T-2 toxin-induced matrix degradation of articular cartilage.

Toxicon. 2023-1-15

[10]
Defective autophagy triggered by arterial cyclic stretch promotes neointimal hyperplasia in vein grafts via the p62/nrf2/slc7a11 signaling pathway.

J Mol Cell Cardiol. 2022-12

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