Histologic examination of the placentas from intrauterine growth retardation (IUGR) fetuses can supplement clinical knowledge of the cause of IUGR. The present study was undertaken to observe the pathologic findings regarding the placentas in IUGR fetuses. Methods : Clinicopathologic findings in 45 cases with IUGR at the third-trimester were reviewed, and they were compared with those of 24 normal control cases. An IUGR fetus was defined as one with a birth weight less than those in the 10th percentile. Of the IUGR cases, 15 were hypertensive IUGR with or without preeclampsia, and 30 were normotensive IUGR. Results : The IUGR groups had significantly shorter mean gestational ages, lower mean placental weights, and higher incidences of oligohydramnios, compared to the normal controls (p<0.05). Histologically, IUGR was characterized by increased incidence of decidual vasculopathy (31.1%, p<0.05), multiple and severe infarct (p<0.05), villous fibrosis (31.1%, p<0.05), syncytiotrophoblastic knots (86.7%, p<0.05), and higher degree of increased perivillous fibrin deposition (p<0.05). However, there were no statistically significant differences in the placental lesions between hypertensive and normotensive IUGR cases, except for the presence of decidual vasculopathy. Conclusions : Abnormal uteroplacental vasculature and chronic uteroplacental insufficiency, coagulation-related pathology in the uteroplacental, intervillous and/or fetoplacental vasculature, and chronic inflammatory lesions may be the primary disease processes related to the placental pathology of IUGR. Although the cause of IUGR pregnancies is heterogeneous, careful cilinicopathologic correlations in individual cases are necessary in the interpretation of placental lesions of IUGR, and the total burden of several placental lesions may be more important than a single histologic feature.

Camptothecin (CPT), which has been used for cancer treatment and apoptosis study, is an extract of Camptotheca acuminata Dence. It is known that CPT induces apoptosis as an inhibitor of DNA topoisomerase I. We investigated the possibility that camptothecin induces anti-apoptotic bcl-2 and pro-apoptotic bax, cytochrome c and caspase-3. Methods : We performed immuocytochemical stains for bcl-2, bax and cytochrome c, and also performed western blots for caspase-3 and the three proteins above using mouse 3T3 fibroblasts treated with CPT (0.5 g/mL). The immunostain for bcl-2 was done 12 hours after a microinjection of antisense oligomer to bcl-2 in the nuclei of the cells. Results : On immunocytochemistry, bcl-2 showed no expressions regardless of CPT treatment and microinjection of the antisense oligomer. The expression of cytochrome c was not changed before and after CPT treatment, and bax demonstrated weak or moderate expressions at 36 and 48 hours after the treatment. There were no expressions at 0, 12, and 24 hours after CPT treatment. On western blot, bcl-2 exhibited no expressions before and after CPT treatment. Expressions of cytochrome c and caspase-3 increased after CPT treatment, and expressions of bax decreased 24 hours after CPT treatment followed by a tendency of increased expressions as time went by. Conclusions : In the CPT-induced apoptosis of mouse 3T3 fibroblasts, CPT induced increased expressions of bax, cytochrome c and caspase-3 with no expressions of bcl-2, which are associated with the apoptosis pathway.