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Antioxidant agents against trichothecenes: new hints for oxidative stress treatment

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...

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Autores principales: Wu, Qinghua, Wang, Xu, Nepovimova, Eugenie, Wang, Yun, Yang, Hualin, Li, Li, Zhang, Xiujuan, Kuca, Kamil
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5746416/
https://www.ncbi.nlm.nih.gov/pubmed/29299181
http://dx.doi.org/10.18632/oncotarget.22800
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author Wu, Qinghua
Wang, Xu
Nepovimova, Eugenie
Wang, Yun
Yang, Hualin
Li, Li
Zhang, Xiujuan
Kuca, Kamil
author_facet Wu, Qinghua
Wang, Xu
Nepovimova, Eugenie
Wang, Yun
Yang, Hualin
Li, Li
Zhang, Xiujuan
Kuca, Kamil
author_sort Wu, Qinghua
collection PubMed
description 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.
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spelling pubmed-57464162018-01-03 Antioxidant agents against trichothecenes: new hints for oxidative stress treatment Wu, Qinghua Wang, Xu Nepovimova, Eugenie Wang, Yun Yang, Hualin Li, Li Zhang, Xiujuan Kuca, Kamil Oncotarget Review 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. Impact Journals LLC 2017-11-30 /pmc/articles/PMC5746416/ /pubmed/29299181 http://dx.doi.org/10.18632/oncotarget.22800 Text en Copyright: © 2017 Wu et al. http://creativecommons.org/licenses/by/3.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.
spellingShingle Review
Wu, Qinghua
Wang, Xu
Nepovimova, Eugenie
Wang, Yun
Yang, Hualin
Li, Li
Zhang, Xiujuan
Kuca, Kamil
Antioxidant agents against trichothecenes: new hints for oxidative stress treatment
title Antioxidant agents against trichothecenes: new hints for oxidative stress treatment
title_full Antioxidant agents against trichothecenes: new hints for oxidative stress treatment
title_fullStr Antioxidant agents against trichothecenes: new hints for oxidative stress treatment
title_full_unstemmed Antioxidant agents against trichothecenes: new hints for oxidative stress treatment
title_short Antioxidant agents against trichothecenes: new hints for oxidative stress treatment
title_sort antioxidant agents against trichothecenes: new hints for oxidative stress treatment
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5746416/
https://www.ncbi.nlm.nih.gov/pubmed/29299181
http://dx.doi.org/10.18632/oncotarget.22800
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