Abstract
Fumonisin B1 (FB1) is among the most common contaminants produced by Fusarium spp. fungus from corns and animal feeds. Although FB1 has been known to cause physical or functional defects of embryos in humans and several animal species such as Syrian hamsters, rabbits, and rodents, little is known about the precise toxicity to the embryos and the underlying mechanisms have not been fully addressed. The present study aimed to investigate its developmental toxicity and potential mechanisms of action on sphingolipid metabolism in Brown Tsaiya Ducks (BTDs) embryos. We examined the effect of various FB1 dosages (0, 10, 20 and 40 µg/embryo) on BTD embryogenesis 72 h post-incubation. The sphingomyelin content of duck embryos decreased (p < 0.05) in the highest FB1-treated group (40 µg). Failure of neural tube closure was observed in treated embryos and the expression levels of a neurulation-related gene, sonic hedgehog (Shh) was abnormally decreased. The sphingolipid metabolism-related genes including N-acylsphingosine amidohydrolase 1 (ASAH1), and ceramide synthase 6 (CERS6) expressions were altered in the treated embryos compared to those in the control embryos. Apparently, FB1 have interfered sphingolipid metabolisms by inhibiting the functions of ceramide synthase and folate transporters. In conclusion, FB1-caused developmental retardation and abnormalities, such as neural tube defects in Brown Tsaiya Duck embryos, as well as are partly mediated by the disruption of sphingolipid metabolisms.
Highlights
Introduction distributed under the terms andFumonisins (FBs), discovered in 1988, are mycotoxins produced by fungi of the Fusarium species including Fusarium verticillioides and Fusarium proliferatum [1,2]
It has been known that 1 toxicity involves in the disturbance of the sphingolipid known that 1 toxicity involves in the disturbance of the sphingolipid metabolisms
It has been known that fumonisin B1 (FB1) toxicity involves in the disturbance of the sphingolipid metabolisms
Summary
Treatments with FB1 did not cause embryo death at 72 h post-incubation (Table 1). Results showed that the viability of embryos was unaffected by the treatment of FB1. FB1 caused a growth retardation and delay of the developmental stage, evaluated by embryonic crown-to-tail length (ECTL) and numbers of somites. The percentages of malformation were higher in the FB1 treated groups compared to the untreated control (0% vs 73.7–88.9%; p < 0.0001). Viability = (No of live embryos/total of embryos) × 100. Embryonic development based on BTD staging system reported by Lumsangkul, et al [32]. 5 Delayed development is compared with the stage of the control group (0 μg). A, b Within the row, means without the same superscripts differ (p < 0.05) Embryonic development based on BTD staging system reported by Lumsangkul, et al [32]. 4 Embryonic crown-to-tail length. 5 Delayed development is compared with the stage of the control group (0 μg). a, b Within the row, means without the same superscripts differ (p < 0.05)
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