Influence of deoxynivalenol on the oxidative status of HepG2 cells.

Abstract

This study was undertaken in order to investigate the effect of deoxynivalenol on the oxidative status and antioxidant defense of HepG2 cells. The HepG2 cells were exposed to 2.5 μM deoxynivalenol for 6, 12 and 24 hours. Higher (p<0.01) activities of the antioxidant enzymes such as superoxide dismutase and catalase were observed after 12 and 24 hours of mycotoxin exposure, while, for the same time points, the superoxide anion level returned to the control values. The present findings imply that the reactive oxygen species that are generated in HepG2 cells due to deoxynivalenol exposure were detoxified by the induction of antioxidant enzymes, such as superoxide dismutase and catalase. The glutathione levels and the activities of the enzymes involved in the metabolism of glutathione, glutathione peroxidase, glutathione-S-transferase and glutathione reductase, were decreased for all times of mycotoxin exposure. This finding suggests that the glutathione cell cycle was seriously perturbed by HepG2 exposure to 2.5 μM deoxynivalenol. The modulation of the two enzymes involved in NADPH synthesis, isocitrate dehydrogenase and glucose6-phosphate dehydrogenase, were time-dependent. At 6 hours, the regeneration of NADPH was provided by isocitrate dehydrogenase, while at 12 hours both enzymes are increased and, finally, at 24 hours, only the activity of glucose-6-phosphate dehydrogenase was up-regulated. These data suggest that an incomplete adaptation of the antioxidant defense system of HepG2 cells occurs in order to minimize oxidative injury caused by deoxynivalenol.