Abstract
Fumonisins are fungal toxins found in corn and in corn-based foods. Fumonisin B1 (FB1) is the most common and is toxic to animals, causes cancer in rodents, and is a suspected risk factor for cancer and birth defects in humans. The hydrolyzed form of FB1 (HFB1) also occurs in foods and is metabolized by rats to compounds collectively known as N-acyl-HFB1 (also known as N-acyl-AP1). N-acyl-HFB1 is structurally similar to ceramides, metabolites which have important structural and signaling functions in cells. FB1 is N-acylated in vitro to ceramide-like metabolites which, like FB1, are cytotoxic. However, metabolism of FB1 and inhibition of ceramide synthase by its metabolites in vivo has not been demonstrated. Male rats were dosed ip with 0.5, 1, or 2 mg/kg body weight FB1 on five consecutive days and the liver and kidney thereafter processed for chemical analysis. N-acyl derivatives of fumonisin B1 were identified for the first time in these principal target organs of FB1 in rats, at levels up to 0.4 nmol/g tissue using mass spectrometry. The N-acyl chain length of the metabolites varied in a tissue-dependent manner with C16 derivatives predominating in the kidney and C24 derivatives being prevalent in the liver. The toxicological significance of N-acyl-fumonisins is not known and warrants investigation.Electronic supplementary materialThe online version of this article (doi:10.1007/s12550-014-0211-5) contains supplementary material, which is available to authorized users.
Highlights
Electronic supplementary material The online version of this article contains supplementary material, which is available to authorized users.H
In order to evaluate the metabolism of fumonisins, the concentrations of Fumonisin B1 (FB1), hydrolyzed form of FB1 (HFB1), and their metabolites were determined in the kidney and liver
The average concentrations of FB1 in the liver were 12- to 20-fold lower. This pattern of preferential accumulation of FB1 in the kidney is consistent with previously published data (Riley and Voss 2006) showing that the FB1 concentration in the kidney of rats fed with fumonisin-contaminated diet was approximately tenfold higher than that in the liver
Summary
Electronic supplementary material The online version of this article (doi:10.1007/s12550-014-0211-5) contains supplementary material, which is available to authorized users. Fumonisins are secondary metabolites of fungi, mainly Fusarium verticillioides and Fusarium proliferatum They were described for the first time by Gelderblom et al (1988) who isolated and characterized fumonisin B1 (FB1) by means of a biosassay based on the promotion of carcinogenesis in rat liver. Mycotoxin Res (2015) 31:33–40 sphinganine and sphingosine, and Wang et al (1991) found that FB1 inhibits ceramide synthase (CerS), a critical enzyme in the de novo biosynthesis of ceramide and complex sphingolipids, and disrupts sphingolipid metabolism. These and subsequent studies have established disrupted sphingolipid metabolism as the mode of action of fumonisins (Bulder et al 2012). We report the in vivo formation of NAFB1 in rats exposed to FB1
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