Abstract
The mycotoxin fumonisin B1 (FB1) is a frequent contaminant of feed. It causes a disruption of sphingolipid metabolism and pulmonary, hepatic, and immunological lesions in pigs depending on the exposure scenario. One sensitive biomarker for FB1 exposure is the sphinganine (Sa) to sphingosine (So) ratio in blood. The fumonisin esterase FumD, which can be used as a feed additive, converts FB1 into the much less toxic metabolite hydrolyzed FB1 (HFB1). We conducted a single-dose study with barrows allocated to one of five treatments: (1) control (feed, 0.9% NaCl intravenously iv), (2) 139 nmol FB1 or (3) HFB1/kg BW iv, (4) 3425 nmol FB1/kg BW orally (po), or (5) 3321 nmol FB1/kg BW and 240 U FumD/kg feed po. The Sa/So ratio of iv and po FB1 administered groups was significantly elevated in blood and Liquor cerebrospinalis, but no fumonisin-associated differences were reflected in other endpoints. Neither clinical lung affections nor histopathological pulmonary lesions were detected in either group, while some parameters of hematology and clinical biochemistry showed a treatment–time interaction. FumD application resulted in Sa/So ratios comparable to the control, indicating that the enzymatic treatment was effectively preventing the fumonisin-induced disruption of sphingolipid metabolism.
Highlights
It was reported by the Food and Agriculture Organization (FAO) that approximately 25% of the world’s agricultural commodities are contaminated with mycotoxins, leading to significant economic losses [1]
The rise in Sa/So ratio was primarily caused by a time-dependent increase in sphinganine concentration upon fumonisin B1 (FB1) -exposure, whereas sphingosine changes were only of minor importance
Levels of sphingoid bases and their ratio detected in the enzyme-treated pigs of group FumDpo, were comparable to those of CON and HFB1iv groups, with no alteration during the course of experiment
Summary
It was reported by the Food and Agriculture Organization (FAO) that approximately 25% of the world’s agricultural commodities are contaminated with mycotoxins, leading to significant economic losses [1]. Different fumonisins have been reported so far and were grouped into main categories A, B, C, and P. (FB1 ), but co-occurrence with other fumonisins (FB2 , FB3 ) as well as other mycotoxins such as aflatoxin or zearalenone is possible [3]. It is described in the literature that fumonisin toxicity is based on a competitive inhibition of sphinganine (sphingosine) N-acyltransferase (ceramide synthase, CerS), a key enzyme in sphingolipid metabolism (Figure S1) [4]. All fumonisins consist of a long hydroxylated hydrocarbon chain linked to tricarballylic acid, methyl, and amino groups [5] and show structural similarity to the original substrates of CerS, sphinganine (Sa), and sphingosine (So)
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