Analysis of pathophysiology of fetal central nerve injury and development for the method of evaluation

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The majour backgrounds for fetal central nerve injury during the course of pregnancy are intrauterine growth retardation (IUGR) and preterm birth. In order to elucidate the effect of oxidative stress on the pathogenesis of IUGR, we measured the amount of 8-oxodeoxyguanine (8-OHdG) in the samples of amniotic fluid and placental genomic DNA. We also examined the expression levels of enzymes Mut-T and Mut-Y, which deeply concern with elimination of 8OHdG from nucleotide pool. The concentration of 8OHdG in the amniotic fluid was lower in the IUGR group than control samples, whereas the 8OHdG amount in the placental chromosomal DNA was equivalent between two groups. The expression levels of Mut-T and Mut-Y mRNA, estimated by RT-PCR, were lower in the placental tissues of IUGR group These result suggested that fetus, rather than placenta are more affected by oxidative stress as pathogenesis of IUGR. Another background of fetal nerve injury should be preterm birth. One of pathophysiology of p … More reterm birth could be premature expression of oxytocin receptor in myometrium. To elucidate the mechanism of this expression, we attempted to clone DNA binding proteins to the oxytocin receptor gene. hMafF, a chicken MafF homologue, was obtained from Yeast one-hybrid screening which has the leucine zipper structure and binds specifically to the oxytocin receptor gene. hMafF mRNA as specifically expressed in term myometrium, whilst the expression during preterm myometrium should further be examined. The knock out mice model could also be an attractive model for investigation of the mechanism of preterm birth. We have literary reviewed the results of mice lacking the genes concerned as the important factor for preterm birth. Many kinds of knock out mice had developed, although most of them appears to be normal on their parturition, i. e., not informative for the investigation of preterm birth.We have analysed several factors for the background of fetal neurological injury. However, we failed to show the direct pathophysiological relationship within the fetal brain. We should develop novel strategy to evaluate fetal brain directly. Less