© 1997 Oxford University Press
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Lack of Embryotoxicity of Fumonisin B1 in New Zealand White Rabbits
*Division of Reproductive and Developmental Toxicology Jefferson, Arkansas 72079-9502
Division of Biochemical Toxicology Jefferson, Arkansas 72079-9502
Division of Biometry and Risk Assessment National Center for Toxicological Research, Food and Drug Administration, Department of Health and Human Services Jefferson, Arkansas 72079-9502
§Center for Food Safety and Applied Nutrition 8301 Muirkirk Road, HFS-507, Food and Drug Administration, Laurel, Maryland 20708
Received January 31, 1997; accepted September 11, 1997
Fumonisin B (FB1) is one of a number of mycotoxins produced by fungi, especially Fusarium sp. As a contaminant of many maizederived products, this toxin is associated with a variety of animal diseases, including esophageal cancer and possibly neural tube defects in humans. We have investigated the embryotoxic potential of this compound in New Zealand White rabbits. Animals were dosed by gavage daily on GD 3–19 with purilied FB1 at 0.10, 0.50, or 1.00 mg/kg/day. Maternal lethality occurred at the 0.50 and 1.00 mg/kg/day doses. When examined on GD 29, there were no differences in maternal body weight, maternal weight gain, maternal organ weights, number of nonlive iinplantations, and number of malformations. Fetal weight was decreased at 0.50 and 1.00 mg/kg/day (13 and 16%, respectively); this was true for male and female pups. Fetal liver and kidney weights were also decreased at these doses. Analysis of embryonic sphinganine to sphingosine ratios demonstrated no differences between control and treated embryos on GD 20, although these ratios were increased in maternal urine, serum, and kidney when compared to control animals. These data suggest that FB1 did not cross the placenta and that the observed decreased fetal weight was probably the result of maternal toxicity, rather than any developmental toxicity produced by FB1.