In vitro and in vivo effects of fumonisins : toxicity and mechanism of action
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概要
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Fumonisins are mycotoxins produced by Fusarium moniliforme (FM), a major worldwide fungal contaminant of corn, and other Fusarium species. Consumption of FMcontaminated corn has been associated with high incidences of human esophageal cancer in sections of China and southern Africa. One fumonisin, fumonisin B1 (FB1), has been shown to cause equine leukoencephalomalacia and porcine pulmonary edema, fatal FM-induced field toxicoses of horses and swine, respectively. Hepatocarcinomas have been found in male rats chronically fed 50ppm FB1. Fumonisins are inhibitors of de novo sphingolipid biosynthesis in vitro and it has been proposed that in vivo toxicity may result from altered sphingolipid metabolism. Diets containing 0, 1, 3, 9, 27, or 81ppm FB1 were fed to rats and mice for 90days. Although previous studies established that FB 1 is hepatotoxic in rats, FB 1 did not cause liver damage to rats in this study. Nephrosis was found in male rats fed ≥ 9 ppm FB 1 and, to a lesser extent, in females fed 81 ppm FB 1. In contrast FB1 was hepatotoxic in female, but not male, mice fed the 81 ppm diets. Thus, the "no observed effect levels, " 3 ppm for rats and 27 ppm for mice, and organ-specific effects differed in the two species. In a second, four-week study, sphingolipid metabolism was altered in male and female rats fed 15, 50, or 150 ppm FB1. The degree of tissue injury as determined by serum chemical and morphological endpoints was correlated with the magnitude of renal, hepatic, and urinary sphingolipid profile alterations. These findings support the hypothesis that sphingolipid metabolism plays a role in FB 1 toxigenesis in vivo. Further studies to compare sphingolipid metabolism and toxicity in rats and mice as well as to further study the in vitro and in vivo effects of fumonisins on sphingolipid metabolism are warranted.
- 日本マイコトキシン学会の論文
日本マイコトキシン学会 | 論文
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