PRENATAL FUMONISIN (FB1) TREATMENT IN RATS RESULTS IN MINIMAL MATERNAL OR OFFSPRING TOXICITY

Citation
Sa. Ferguson et al., PRENATAL FUMONISIN (FB1) TREATMENT IN RATS RESULTS IN MINIMAL MATERNAL OR OFFSPRING TOXICITY, Neurotoxicology, 18(2), 1997, pp. 561-569
Citations number
26
Categorie Soggetti
Pharmacology & Pharmacy",Neurosciences
Journal title
ISSN journal
0161813X
Volume
18
Issue
2
Year of publication
1997
Pages
561 - 569
Database
ISI
SICI code
0161-813X(1997)18:2<561:PF(TIR>2.0.ZU;2-6
Abstract
To investigate the neurobehavioral and developmental effects of the my cotoxin, FB1, Sprague-Dawley rats were treated with FB1 on gestational days 13-20. In Experiment I, FB1 was obtained from culture material a nd pregnant rats were gavaged with 0, 0.8 or 1.6 mg/kg. In Experiment 2, pregnant rats were gavaged with purified FB1 at doses of 0, 1.6 or 9.6 mg/kg. Offspring were evaluated on a battery of behavioral tests a s well as measures of whole and regional brain weight. There were no e ffects on maternal weight gain, reproductive outcomes, or offspring bo dy weight through adulthood in either experiment. Complex maze perform ance, open field and running wheel activity were not altered by prenat al FB1 treatment. In Experiment 2, acoustic startle response was depre ssed at two ages during the first or second block of 9 trials in males treated with purified FB1. Females exhibited no such alterations. Pla y behavior at PND 33, but not PND 26, was increased in males prenatall y treated with 9.6 mg/kg relative to those treated with 1.6 mg/kg. The re were no substantive treatment effects on regional brain weight. The se results suggest that doses of less than or equal to 9.6 mg purified FB1/kg and/or less than or equal to 1.6 mg FB1/kg obtained from cultu re material cause minimal maternal toxicity and produce few developmen tal functional alterations. In addition, potential FB1-related functio nal alterations were evident only in males providing further support f or a mild sex-specific effect for fumonisin. (C) 1997 Inter Press, Inc .