Fumonisin B1 alters sphingolipid metabolism and tumor necrosis factor α expression in heart and lung of mice

Fumonisin B1 (FB1), produced by Fusarium verticillioides, is a common contaminant in foods and feeds. Increase in tissue free sphingoid bases resulting from the inhibition of ceramide synthase is a biomarker of fumonisin exposure. Tumor necrosis factor α (TNFα) is induced in liver in response to FB1 treatment. This study determined whether fumonisin B1 caused increases in free sphingoid bases and altered the expression of TNFα in heart and lung, organs that are not targets of FB1 toxicity, of male and female mice treated with 5-daily subcutaneous injection of 2.25 mg/kg FB1. A significant increase in free sphingoid bases was observed in both heart and lung of FB1-exposed mice. The magnitude of increases in free sphingoid bases in both organs of female mice was much higher than that in males. The expression of TNFα was increased by FB1 treatment in the lung of male mice and in the heart of female mice, whereas the expression of interferon γ was unaltered. Results suggest that both sphingolipid accumulation and TNFα induction are observed in the tissues of mice that are not associated with FB1 toxicity.