Ochratoxin A (OTA), a mycotoxin produced by Aspergillus ochraceus and other moulds, has recently received growing attentionbecause of its carcinogenic, teratogenic and nephrotoxic properties in both humans and farm animals. Nevertheless, with regard to themechanism of toxicity, the data in the literature are inconclusive. The aim of our work was to verify in human fibroblasts treated withdifferent OTA dosages the involvement of oxidative pathway in the damage mechanism of this mycotoxin and the possible protective effectexerted by cyanidin 3-O-h-d-glucoside (C3G), an anthocyanin present in pigmented oranges, red wines, fruits and vegetables.The addition of OTA at 25 and 50 AM concentrations for 48 h determined only a slight but significant ( P b.05) increase in radical oxygenspecies, whereas a substantial increase in their production was observed at longer exposure, in particular, when the fibroblasts were treatedwith 50 AM OTA for 72 h. Under the same experimental conditions, our data showed a significant ( P b.05) increase in the rupture of cellularmembrane and high damage to genomic DNA, evaluated by single-cell gel electrophoresis (comet assay), thus confirming the involvement ofoxidative stress in the OTA genotoxicity in agreement with other studies. Diversely, mitochondrial functionality does not appear influencedby OTA treatment. C3G (0.125, 0.250 mM) added to the cells treated with 50 AM OTA significantly reduced free radical species productionand prevented genomic DNA damage.
|Titolo:||Ochratoxin A-induced DNA damage in human fibroblast: protective effect of cyanidin 3-o-β-d-glucoside|
|Data di pubblicazione:||2005|
|Appare nelle tipologie:||1.1 Articolo in rivista|