1. Fumonisin B(1) alters sphingolipid metabolism and tumor necrosis factor alpha expression in heart and lung of mice.
- Author
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He Q, Bhandari N, and Sharma RP
- Subjects
- Animals, Carboxylic Acids administration & dosage, Carcinogens, Environmental administration & dosage, Female, Injections, Subcutaneous, Interferon-gamma metabolism, Lung metabolism, Male, Mice, Mice, Inbred BALB C, Myocardium metabolism, RNA, Messenger metabolism, Reverse Transcriptase Polymerase Chain Reaction, Sex Factors, Tumor Necrosis Factor-alpha genetics, Carboxylic Acids toxicity, Carcinogens, Environmental toxicity, Fumonisins, Heart drug effects, Lung drug effects, Sphingosine analogs & derivatives, Sphingosine metabolism, Tumor Necrosis Factor-alpha metabolism
- Abstract
Fumonisin B(1) (FB(1)), 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 alpha (TNFalpha) is induced in liver in response to FB(1) treatment. This study determined whether fumonisin B(1) caused increases in free sphingoid bases and altered the expression of TNFalpha in heart and lung, organs that are not targets of FB(1) toxicity, of male and female mice treated with 5-daily subcutaneous injection of 2.25 mg/kg FB(1). A significant increase in free sphingoid bases was observed in both heart and lung of FB(1)-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 TNFalpha was increased by FB(1) treatment in the lung of male mice and in the heart of female mice, whereas the expression of interferon gamma was unaltered. Results suggest that both sphingolipid accumulation and TNFalpha induction are observed in the tissues of mice that are not associated with FB(1) toxicity.
- Published
- 2002
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