Special Issue "Ochratoxins 2011-2012"

Guest Editor
Prof. Dr. Richard A. Manderville
Department of Chemistry and Toxicology, University of Guelph, Guelph, Ontario, N1G 2W1 Canada
Website: http://www.chemistry.uoguelph.ca/manderville/webpage.htm
E-Mail: rmanderv@uoguelph.ca
Phone: +1 519 824 4120
Fax: +1 519 766 1499
Interests: DNA damage by phenolic toxins including ochratoxin A; Modified DNA bases as fluorescent probes

Guest Editor
Prof. Dr. Annie Pfohl-Leszkowicz
National Agronomical High School of Toulouse (ENSAT), Unit of Toxicology & Food safety, 1 avenue de l’Agrobiopôle, BP 32607, 31326, Auzeville-Tolosane, France
E-Mail: leszkowicz@ensat.fr
Phone: + 33 562 193 947
Fax: + 33 562 193 947
Interests: mycotoxin; ochratoxin; fumonisin; zearalenone; biomarker; risk evaluation; environmental toxicology; polycyclic aromatic compounds; genotoxicity; DNA adduct; balkan endemic nephropathy; kidney cancer; biotransformation

Dear Colleagues,

In 2010 a special issue of Toxins entitled “Ochratoxins” published 31 papers concerned with detection of ochratoxins in feed and human foodstuff, occurrence and estimation of dietary intake, and understanding mechanisms of toxicity and carcinogenicity for the development of detoxification processes. In terms of ochratoxin A (OTA) carcinogenicity, highlights from the special issue include the findings by Stoev that OTA induces renal tumors in chicks. Schwartz and coworkers demonstrated that in utero exposure to OTA causes adducts in the testicular DNA of male offspring in support of a possible role for OTA in testicular cancer. 2010 also saw Mantle and coworkers publish convincing evidence that part of the mechanism of OTA carcinogenesis involves direct covalent interaction with DNA.  In the special issue Mantle and Nolan raised new questions about a difference between young adults and mature adults in sensitivity of male rats to the ochratoxin A-induced DNA damage necessary for renal carcinogenesis.  Several papers that include those by Fusi, Varga, Abrunhosa, and Perez examined control strategies for reducing or preventing OTA-induced toxicoses. For OTA detection, Yu and Lai outlined recent advances of molecularly imprinted polymers (MIPs) for the extraction and analysis of ochratoxins. Rapid and reliable visual tests for OTA detection was reviewed by Bazin and coworkers, while a new ELISA test for OTB detection was described by Dietrich coworkers. Numerous other studies demonstrated the wide-spread occurrence of OTA, highlighting that problematic exposure to the toxin is not limited to the Balkan region. Given the level of participation and interest in the special issue “Ochratoxins”, the editorial board of Toxins was eager to run this special issue again. To the many authors that contributed to ‘Ochratoxins” we wish to thank you for sharing your research findings that made the special issue such a success. We hope that this second special issue of Toxins entitled “Ochratoxins 2011” further highlights the ongoing interdisciplinary research on the ochratoxins and provides the readership with a further understanding of the key issues being addressed at the present time.

Prof. Dr. Richard A. Manderville
Prof. Dr. Annie Pfohl-Leszkowicz
Guest Editors

Submission

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed Open Access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 500 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.

Related Special Issues in other Journals

Ochratoxins in Toxins

Submission

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed Open Access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 500 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.

• ochratoxins
• mycotoxin
• carcinogen
• Balkan endemic nephropathy
• DNA damage
• genotoxic
• intake
• biotransformation
• risk assessment

Type of Paper: Review
Title: Pro-Oxidant Effect of Ochratoxin A in Monogastric Animals
Authors: Luisa Pozzo ¹, Laura Cavallarin ² and Achille Schiavone ³
Affiliations: ¹ IBBA-CNR (UOS Pisa), Via Moruzzi 1–56124 Pisa, Italy
² ISPA-CNR, Via L. da Vinci 44–10095 Grugliasco (TO), Italy
³ Dipartimento di Produzioni Animali, Epidemiologia ed Ecologia, Via L. da Vinci 44–10095 Grugliasco (TO), Italy; E-Mail: achille.schiavone@unito.it
Abstract: Ochratoxin A (OTA), is a mycotoxin frequently present in feedstuff. OTA exhibits a wide range of toxic effects such as nephrotoxicity, genotoxicity, immunotoxicity, carcinogenicity and teratogenicity. The mechanism involved in the toxicity of OTA  has three major effects: 1. the inhibition of mitochondrial respiration correlated with a depletion of ATP, 2. the inhibition of tRNA-synthetase followed by a reduced protein synthesis and 3. the enhanced oxidative damage. OTA induces oxidative damage  either directly, by stimulating the formation of a Fe³⁺-OTA complex that may promote reactive oxygen species generation and lipid peroxidation, and indirectly, by lowering the antioxidant and xenobiotic metabolizing enzymes. This article will review the current knowledge about the in vivo and in vitro OTA pro-oxidant activity in rat, pig and chicken.

Title: Mutant Frequency in Comparison to Oxidative DNA Damage Induced by Ochratoxin A in L5178Y/Tk^+/--3.7.2C Mouse Lymphoma Cells
Authors: Rahat Ali ^1,2, Javed A Bhalli ¹ , Xiaoqing Guo ¹, Muhammad Ismail ² and Qaiser M. Khan ^2,*
Affiliations: ¹ National Center for Toxicological Research, U.S. Food and Drug Administration, Jefferson Arkansas, USA; E-Mail: Javed.Bhalli@fda.hhs.gov (J.A.B.)
² National Institute for Biotechnology and Genetic Engineering (NIBGE), Faisalabad, Pakistan; E-Mail: qaiser.khan@nibge.org (Q.M.K.)
Abstract: Ochratoxin A (OTA) is a naturally occurring mycotoxin that contaminates animal feed and human food supplies. OTA is nephrotoxic, hepatotoxic, immunosuppressive, and a potent renal carcinogen in rodents. In this study, we evaluated the genotoxicity of OTA in L5178Y/Tk^+/--3.7.2C mouse lymphoma cells using the microwell version of the mouse lymphoma gene mutation assay and the Comet assay modified to detect oxidative DNA damage. Cells were treated for 4 hr with 5 to 100 µM OTA in the presence and absence of S9. OTA treatment produced dose-dependent increases in cytotoxicity and Tk mutant frequency, with positive increases in mutant frequency detected at concentrations >25 µM with S9 and >50 µM without S9. Similarly treated cells were used for the Comet assay conducted with and without formamidopyrimidine-DNA glycosylase (fpg) for the determination of oxidative DNA damage. OTA exposure resulted in significant increases in both direct and oxidative DNA damage, with the induction of oxidative damage being greater. The results indicate that OTA is a mutagen in the mouse lymphoma assay, that S9 activation has only a modest effect upon its mutagenicity, and that OTA-generated oxidative DNA damage is at least partially responsible for its mutagenicity in the assay.