Fumonisins: oxidative stress-mediated toxicity and metabolism in vivo and in vitro
Language English Country Germany Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
26419546
DOI
10.1007/s00204-015-1604-8
PII: 10.1007/s00204-015-1604-8
Knihovny.cz E-resources
- Keywords
- Antioxidants, DNA damage, Fumonisins, Lipid peroxidation, Metabolism, Metabolizing enzymes, Oxidative stress, Reactive oxygen species,
- MeSH
- Biotransformation MeSH
- Fumonisins metabolism toxicity MeSH
- Fusarium metabolism MeSH
- Risk Assessment MeSH
- Zea mays microbiology MeSH
- Humans MeSH
- Oxidation-Reduction MeSH
- Oxidative Stress drug effects MeSH
- Lipid Peroxidation drug effects MeSH
- DNA Damage MeSH
- Food Microbiology * MeSH
- Reactive Oxygen Species metabolism MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Fumonisins MeSH
- Reactive Oxygen Species MeSH
Fumonisins (FBs) are widespread Fusarium toxins commonly found as corn contaminants. FBs could cause a variety of diseases in animals and humans, such as hepatotoxic, nephrotoxic, hepatocarcinogenic and cytotoxic effects in mammals. To date, almost no review has addressed the toxicity of FBs in relation to oxidative stress and their metabolism. The focus of this article is primarily intended to summarize the progress in research associated with oxidative stress as a plausible mechanism for FB-induced toxicity as well as the metabolism. The present review showed that studies have been carried out over the last three decades to elucidate the production of reactive oxygen species (ROS) and oxidative stress as a result of FBs treatment and have correlated them with various types of FBs toxicity, indicating that oxidative stress plays critical roles in the toxicity of FBs. The major metabolic pathways of FBs are hydrolysis, acylation and transamination. Ceramide synthase, carboxylesterase FumD and aminotransferase FumI could degrade FB1 and FB2. The cecal microbiota of pigs and alkaline processing such as nixtamalization can also transform FB1 into metabolites. Most of the metabolites of FB1 were less toxic than FB1, except its partial (pHFB1) metabolites. Further understanding of the role of oxidative stress in FB-induced toxicity will throw new light on the use of antioxidants, scavengers of ROS, as well as on the blind spots of metabolism and the metabolizing enzymes of FBs. The present review might contribute to reveal the toxicity of FBs and help to protect against their oxidative damage.
College of Life Science Yangtze University Jingzhou China
Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety Wuhan Hubei China
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