engleski

Recent studies on the mechanism of fumonisin B1 toxicity

Fumonisin B1 (FB1) is the most toxic mycotoxin of the fumonisins family produced by the Fusarium moulds. It contaminates grains (mostly maize and wheat) in mild climatic zones. In studies performed on maize samples collected in Croatia the concentration of FB1 was low, not exceeding the maximal allowed concentration for the EU countries. However, very high frequency of FB1-positive samples found in our study as well as the co-contamination with other mycotoxins, such as ochratoxin A, fumonisin B2 and zearalenone makes the problem of FB1 contamination more serious. The most common mycotoxicoses in domestic animals caused by FB1 are leukoencephalomalacia in horses and pulmonary oedema in pigs. It has been established that FB1 has nephrotoxic (rats) and hepatotoxic (mice) properties in laboratory animals. These toxic effects are probably due to the inhibition of enzyme ceramide synthase with the consequent accumulation of sphingolipid sphinganine. The increased ratio of sphinganine and sphingosine (Sa/So) is a valuable parameter for FB1 exposure because FB1 has a very short half-life in blood circulation and FB1 measurements in biological material do not correspond to exposure. FB1 was also found to be genotoxic in various cultured cells, but the mechanism of genotoxicity is not fully understood. Our studies were performed in order to elucidate the mechanism of FB1 genotoxicity in experimental animals (particularly in kidney). In one study the results of Fpg-modified and standard comet assay were compared with antioxidative enzymes in rats treated for 5 days and showed that DNA lesions were only partly caused by oxidative stress. In a time-course study of FB1 treated rats, the catalytic activity of antioxidative enzymes as well as the concentration of protein carbonyls, malondialdehyde (MDA) and Sa and So in plasma, liver and kidney homogenates were compared with the results of the standard comet assay in liver and kidney homogenates. Our results showed that FB1 genotoxicity was not the result of oxidative stress, because its effects on anitoxidative enzymes, protein carbonyls and MDA appeared after DNA lesions. It rather seems that DNA lesions are the result of the disturbance in the sphingolipid metabolism.

fumonisin B1; oxidative stress; comet assay

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