Abstract
Fumonisins are mycotoxins that contaminate maize and wheat. The most toxic and the most frequently found fumonisin is fumonisin B1 (FB1) involved in several animal diseases and supposed to be involved in the etiology of some human tumors. FB1 disturbs the metabolism of sphinganine (Sa) and sphingosine (So) increasing the ratio of their concentrations (Sa/So). FB1 was shown to be mutagenic in several studies on cultured cells. Literature data on the studies of FB1 genotoxicity in experimental animals are rather scarce and the mechanism of genotoxicity is not understood. The aim of this study was to elucidate whether DNA lesions in kidney and liver cells of FB1 treated rats are related to changes of oxidative status. Adult male Wister rats were receiving either FB1 dissolved in sterile saline (0.9 % NaCl) (0.5 mg/kg b.w./day) or solvent only (negative control animals) intraperitoneally for two or seven consecutive days and sacrificed 24 h after the last treatment. Ratio of Sa and So concentrations and parameters of oxidative status (activity of catalase, and concentration of protein carbonyls and malondialdehyde – MDA) were measured in plasma, liver and kidney homogenate, while comet assay was performed in liver and kidney. In plasma and homogenates of liver and kidney activity of catalase, concentration of protein carbonyls and MDA were not affected after two days treatment with FB1. At this time point the ratio of Sa and So in all tested samples was increased. After two days treatment tail length and tail intensity measured with comet assay in liver homogenate was not changed, while in kidney they where significantly different from controls. After seven days treatment all measured parameters were significantly different from controls. This study showed that in experimental animals FB1 causes DNA lesions in kidney before affecting catalytic activity of catalase and concentration of protein carbonyls and MDA. In this time point the ratio of Sa and So significantly increases in all tissues. These results taken together confirm that oxidative stress is the consequence and not the cause of DNA damage and that the metabolism of sphingolipids should be involved in the DNA damage caused by FB1 rather than oxidative stress.
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