Abstract
Fumonisins B 1 and B 2 (FB 1 and FB 2) are fungal secondary metabolites produced by members of the genus Fusarium. Although FB 1 is usually detected in greater quantities, FB 2 frequently co-occurs in contaminated feeds and foods and contributes to the total toxin load. In the present study, the comparative toxicity of FB 1 and FB 2 was examined in male Sprague–Dawley rats administered toxin (0.75 mg/kg body weight) or vehicle control intraperitoneally (ip) for 2, 4 or 6 consecutive days. Clinical changes, including elevated serum cholesterol, alanine aminotransferase (ALT), creatinine and protein, were slightly more pronounced in FB 1-treated rats. The most consistent hematological change was an increase in vacuolated bone marrow cells, which was more pronounced in FB 1-treated rats. Histopathological changes were similar in FB 1- and FB 2-treated rats and included single cell necrosis in kidneys and liver, cytoplasmic vacuolation in adrenal cortex and lymphocytolysis in thymus. In the liver mRNA expression for the cyclin kinase inhibitor p21 gene was significantly increased in FB 1- and FB 2-treated rats, compared to controls. Expression of mRNA for the cyclin D1 gene was significantly depressed in FB 2-treated rats. Hepatic cyclin E mRNA was elevated in response to FB 1 and FB 2 compared to controls. In FB 2-treated animals this corresponded with decreased liver p27 mRNA expression. Hepatic proliferating cell nuclear antigen (PCNA) transcription was elevated in FB 1- but not FB 2- treated rats. Changes in liver microsomal protein levels of p27, cyclin E and PCNA were similar to changes in gene expression. In contrast, cyclin D1 protein levels were elevated in rats treated with FB 1 and, to a lesser extent, FB 2. The data indicate that FB 1 and FB 2 can alter the expression of genes associated with the cell cycle, and indicate a need for a further understanding of the mechanistic basis of FB 1 and FB 2 toxicity.
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