Effects of the prenatal ochratoxin A exposure on behaviors of rat offspring

The effbcts of prenatal ochratoxin A (OCA) exposure on postnatal behavior and function of Jcl: Wistar rat offspring were assessed in two experiments. In Experiment 1, pregnant rats were administered ora]ly with O.25 or O.5 mglkglday of OCA dissolved in O.1 M sodium bicarbonate on days 11-14 (A) or 15-18 (B) of gestation. Controls received the vehicle similarly on days 11-18 of gestation. The offSpring were examined by preweaning and postweaning behayioral tests. In the preweaning test, the offSpring in the O.25 and O.5 mg/kg-A groups showed significantly lower success rates than controls in surface righting reflex. Those in the O.5 mgl kg-A and B groups also showed significantly lower success rates in negative geotaxis. In the swimming test, the offspring in all OCA-treated groups had significantly lower scores than controls for body angle, and in the O.25 mglkg-A group the scores for swimming direction were significantly tower than those of controls. In postweaning tests, ayoidance 1earning task of the rats in the O.25 and O.5 mg/kg-A groups was signifioantly poorer than that of controls. In order to clarify whether the behavioral alteration in the offspring was due to direct effbcts on embryos or to the indirect effbcts on the mothers, neonatal rats were cross-fostered in Experiment 2. Pregnant rats were administered orally with e or O.5 mglkg!day of OCA on days 11-14 of gestation. In the aequisition of avoidance response, the avoidance rates of OCA-treated offirpring were significantly lower than those of either the control offspring fostered by other control mothers or the control offspring fostered by OCA-treated mothers. In the extinction of the ayoidance response, OCA-treated offspring showed significant)y higher ayoidance rates compared with either contro] offspring fbstered by other contro] mothers or control offspring fostered by OCA-treated mothers. These results indicate that prenatal exposure to OCA produoed a de]ay of early reflex deyelopment and learning deficiencies. The doses required to induce behavioral disorders were much lower than that to cause death, gross malformations or growth retardation. These behavioral effects were more pronounced during mid-organogenesis (days 11-14) than in Iate organogenesis (days 15-18), and OCA also produced long lasting impairments of avoidance 1earning in mature animals. Furthermore, it was demonstrated that learning dysfunctions in the offSpring are not of materna] origin but dlle to the direct effects of OCA on embryos in utero.