Ochratoxin A and DNA damage

Related tags Kidney

How, and why, can exposure to ochratoxin A result in DNA damage and
tumour induction? A new EU-funded project at the university of
Würzburg in Germany, will aim to answer these questions.

How, and why, can exposure to ochratoxin A result in DNA damage and tumour induction? A new EU-funded project at the university of Würzburg in Germany, will aim to answer these questions.

Co-ordinated by Dr. Wolfgang Dekant the project hopes to obtain crucial information on the dose-response curve for ochratoxin A-induced toxic effects. In addition, it aims to improve understanding of the mechanisms resulting in DNA damage and its contributions to tumour induction by ochratoxin A. This, in turn, will serve as a basis for establishing scientifically sound maximum permitted levels for ochratoxin A within the EU. The new German project is in fact part of a larger cluster of EU projects revolving around mycotoxins

Ochratoxin A is a mycotoxin which can contaminate a number of foods, such as grapes, cereals, animal products, and even coffee and beer. Human exposure is inevitable, and ochratoxin A has been detected in human blood samples, but generally at low levels in healthy people. Low levels of ochratoxin A in foods are not considered to pose a risk to health at all, however, at high levels it is considered to be a potential carcinogen. Animal studies have shown that a type of ochratoxin A can cause tumours in the kidney and other organs. In humans, exposure to high levels of ochratoxin A has been linked with chronic renal disease and an increased incidence of urinary tract tumours.

Results so far from rat studies suggest that exposure to ochratoxin A in feed, for a period of six months, resulted in slight, but consistent, modification in terms of genetic damage in some tissues and organs. Scientists working in the cluster report that the induction of primary DNA lesions has also been observed in liver and bone marrow cells, but at this stage it is not possible to say whether these lesions are induced by oxidative stress or generated by adducts to DNA of ochratoxin A metabolites.

Progress on the German study can be tracked on the university's website​.

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