Ochratoxin A causes DNA damage in rats kidney

Abstract

Ochratoxin A (OTA) is product of moulds frequently found in food and feed in mild climatic zones. This mycotoxin was found to be nephrotoxic for experimental animals and the carcinogenic potential of OTA in kidney of experimental animals is well established. The results of OTA genotoxic potential on cell cultures are inconsistent and the studies on genotoxicity in experimental animals are scarce. The aim of this study was to assess the time-course of OTA-produced DNA damage by checking alkali-labile sites using the comet assay of rat kidney tissue. Rats were treated intraperitoneally with OTA (0.5 mg/kg b.w./day for 7, 14, and 21 days, respectively) and sacrificed 24 hours after the last treatment. Positive controls were given methyl methanesulfonate and negative controls solvent only following the same schedule of treatment. The genotoxic potential of OTA was studied in the kidney homogenate of OTA treated and control rats using alkaline single-cell gel electrophoresis (comet assay). Concentrations of OTA in plasma and kidney homogenate were determined using high performance liquid chromatography. OTA concentrations in plasma and kidney tissue increased steadily during the treatment period. In all OTA-treated groups, the tail length, tail intensity, and tail moment in the kidney tissue were significantly higher than in controls (P<0.05). The tail length and tail moment were higher after 14 days than after 7 days of treatment (P<0.05), and still higher after 21 days than after 7 and 14 days (P<0.05). The highest tail intensity was observed in animals treated for 21 days, and it differed significantly from animals treated for 7 and 14 days (P<0.05). OTA concentration measured in the kidney tissue strongly correlated with the tail intensity and tail moment values. These results confirm the genotoxic potential of OTA, which is in accordance with its carcinogenicity.