engleski

The involvement of oxidative stress in fumonisin B1 genotoxicity

Fumonisin B1 (FB1) is mycotoxin produced by variety of Fusarium fungi, common fungal contaminants of maize worldwide. Several studies in Croatia demonstrated high contamination of maize with this mycotoxin. FB1 causes leukoencephalomalacia in horses and pulmonary oedema in pigs and is nephrotoxic, hepatotoxic and carcinogenic to rats and mice. Human exposure to corn-based food contaminated with FB1 has been connected to esophageal cancer, primary liver cancer and neural tube defect. It has been established that FB1 toxic effect is consequence of disruption of sphingolipid metabolism. Disruption results in inhibition of de novo ceramide biosynthesis, and accumulation of free sphingoid bases. Genotoxic effect of FB1 was studied on various cells lines, but the mechanism of its genotoxicity is not fully understood. Several experiments aimed to elucidate weather oxidative stress is involved in the mechanism of FB1 genotoxicity were performed. In one study on rats treated for 5 days with various FB1 doses (200 ng/kg, 50  g/kg and 500 g/kg b.w., respectively) standard and Fpg-modified comet assay in kidney cells indicated that DNA lesions were only partly caused by oxidative stress. In another study when rats were treated with FB1 for 2 and 7 days (500  g/kg b.w.) changes of parameters of oxidative stress (catalase, protein carbonyls and malondialdehyde) appeared after DNA lesions as measured with standard comet assay. In short-term study on rats treated with 5, 50 and 500 g/kg b.w., respectively and sacrificed 4, 24 and 48 h afterwards, it was demonstrated that DNA lesions caused by FB1 measured with standard comet assay are dose- and time-dependent and appeared after changes in sphingolipid metabolism. It seems that DNA lesions are primarily result of the disturbance in the sphingolipid metabolism rather than oxidative stress.

fumonisin B1; catalase; protein carbonyls; malondialdehyde

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