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Ochratoxin A: 50 Years of Research
F. Malir, V. Ostry, A. Pfohl-Leszkowicz, J. Malir, J. Toman,
Language English Country Switzerland
Document type Historical Article, Journal Article, Review, Research Support, Non-U.S. Gov't
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PubMed
27384585
DOI
10.3390/toxins8070191
Knihovny.cz E-resources
- MeSH
- Balkan Nephropathy chemically induced genetics history metabolism MeSH
- History, 20th Century MeSH
- History, 21st Century MeSH
- Epigenesis, Genetic drug effects MeSH
- Risk Assessment MeSH
- Kidney drug effects metabolism pathology MeSH
- Humans MeSH
- Cell Transformation, Neoplastic chemically induced genetics metabolism MeSH
- Kidney Neoplasms chemically induced genetics history metabolism MeSH
- Ochratoxins history metabolism toxicity MeSH
- Oxidative Stress drug effects MeSH
- DNA Damage MeSH
- Food Microbiology * history trends MeSH
- Gene Expression Regulation, Neoplastic drug effects MeSH
- Risk Factors MeSH
- Toxicology * history trends MeSH
- Animals MeSH
- Check Tag
- History, 20th Century MeSH
- History, 21st Century MeSH
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Historical Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
Since ochratoxin A (OTA) was discovered, it has been ubiquitous as a natural contaminant of moldy food and feed. The multiple toxic effects of OTA are a real threat for human beings and animal health. For example, OTA can cause porcine nephropathy but can also damage poultries. Humans exposed to OTA can develop (notably by inhalation in the development of acute renal failure within 24 h) a range of chronic disorders such as upper urothelial carcinoma. OTA plays the main role in the pathogenesis of some renal diseases including Balkan endemic nephropathy, kidney tumors occurring in certain endemic regions of the Balkan Peninsula, and chronic interstitial nephropathy occurring in Northern African countries and likely in other parts of the world. OTA leads to DNA adduct formation, which is known for its genotoxicity and carcinogenicity. The present article discusses how renal carcinogenicity and nephrotoxicity cause both oxidative stress and direct genotoxicity. Careful analyses of the data show that OTA carcinogenic effects are due to combined direct and indirect mechanisms (e.g., genotoxicity, oxidative stress, epigenetic factors). Altogether this provides strong evidence that OTA carcinogenicity can also occur in humans.
References provided by Crossref.org
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- $a Malir, Frantisek $u Department of Biology, Faculty of Science, University of Hradec Kralove, Hradec Kralove 50003, Czech Republic. frantisek.malir@uhk.cz.
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- $a Since ochratoxin A (OTA) was discovered, it has been ubiquitous as a natural contaminant of moldy food and feed. The multiple toxic effects of OTA are a real threat for human beings and animal health. For example, OTA can cause porcine nephropathy but can also damage poultries. Humans exposed to OTA can develop (notably by inhalation in the development of acute renal failure within 24 h) a range of chronic disorders such as upper urothelial carcinoma. OTA plays the main role in the pathogenesis of some renal diseases including Balkan endemic nephropathy, kidney tumors occurring in certain endemic regions of the Balkan Peninsula, and chronic interstitial nephropathy occurring in Northern African countries and likely in other parts of the world. OTA leads to DNA adduct formation, which is known for its genotoxicity and carcinogenicity. The present article discusses how renal carcinogenicity and nephrotoxicity cause both oxidative stress and direct genotoxicity. Careful analyses of the data show that OTA carcinogenic effects are due to combined direct and indirect mechanisms (e.g., genotoxicity, oxidative stress, epigenetic factors). Altogether this provides strong evidence that OTA carcinogenicity can also occur in humans.
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- $a Pfohl-Leszkowicz, Annie $u Department Bioprocess & Microbial Systems, Laboratory Chemical Engineering, INP/ENSA Toulouse, University of Toulouse, UMR 5503 CNRS/INPT/UPS, Auzeville-Tolosane 31320, France. leszkowicz@ensat.fr.
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