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Comments on “Ochratoxin A: In utero Exposure in Mice Induces Adducts in Testicular DNA. Toxins 2010, 2, 1428–1444”—Mis-Citation of Rat Literature to Justify a Hypothetical Role for Ochratoxin A in Testicular Cancer
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Reply of Toxins 2010, 2(10), 2333-2336.

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Toxins 2010, 2(10), 2337-2339; doi:10.3390/toxins2102337

Response to Comments of Peter G. Mantle

Departments of Cancer Biology, Urology, and Epidemiology and Prevention, Wake Forest University, Winston-Salem, NC 27157, USA
Department of Chemistry and Toxicology, University of Guelph, Guelph, Ontario, N1G 2W1, Canada
University of Toulouse, Laboratory Chemical Engineering, Department Bioprocess & Microbial System, UMR CNRS/INPT/UPS 5503, ENSA Toulouse, 1 avenue de l’Agrobiopôle, BP 32607, 31326, Auzeville-Tolosane, France
Author to whom correspondence should be addressed.
Received: 17 September 2010 / Accepted: 28 September 2010 / Published: 29 September 2010
(This article belongs to the Special Issue Ochratoxins)
View Full-Text   |   Download PDF [24 KB, uploaded 29 September 2010]


The apparently high yield of testis tumors (25%) in rats exposed long-term to Ochratoxin A (OTA) is uninterpretable without data on tumor yield in unexposed rats. Conversely, our demonstration that prenatal exposure to OTA induces DNA adducts in the testes of newborn mice and the absence of these adducts in the testes of mice not exposed prenatally to OTA, is evidence for the presumptive carcinogenicity of OTA in the testis. Together with recent data showing that prenatal exposure to OTA depresses expression of DMRT1, a tumor suppressor gene in the testis, our findings suggest that OTA may be a cause of testicular cancer.
Keywords: ochratoxin; testicular cancer; DNA adduct ochratoxin; testicular cancer; DNA adduct
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Schwartz, G.G.; Manderville, R.A.; Pfohl-Leszkowicz, A. Response to Comments of Peter G. Mantle. Toxins 2010, 2, 2337-2339.

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