EFFECTS OF POLYAROMATIC COMPOUNDS ON PLACENTAL PROTEINS

描述：(改编自《调查员摘要》)目标 这项拟议的研究旨在阐明细胞和生化变化。 胎盘是胎儿胎盘发育迟缓的基础 与接触多环芳烃(PAH)有关 怀孕了。第一个具体目标将调查暴露在 人胎盘细胞对苯并(A)芘(BP)及其相关多环芳烃化合物的作用 改变滋养层细胞的分化。提出了实验方案。 定量测定BP对细胞滋养层融合形成合胞体的影响 以及分化的生化标记物的表达， 绒毛膜促性腺激素(HCG)、胎盘催乳素(HPL)和 妊娠特异性B1糖蛋白(HPSBG)。BP对表皮生长因子的影响 将检查受体以确定受体的下调是否 与分化状态的变化在时间上相关。第二 特定目标将检查大鼠胎盘以确定是否暴露于 原型多环芳烃化合物改变生长因子的产生或受体 在母胎交界处发挥作用。研究将确定是否 BP，B-萘黄酮(BNF)3-甲基胆蒽，(3mc)和 2，3，7，8-四氯二苯并对二恶英(TCDD)对 滋养层细胞，或者滋养层细胞是否被间接改变 母体蜕膜细胞因子产生的变化。最终的具体内容 目的是评估细胞因子，特别是IL-1是否调节 细胞色素P-450IA1在胎盘细胞中的诱导

DESCRIPTION: (Adapted from the Investigator's Abstract) The objective of the proposed research is to elucidate cellular and biochemical alterations in the placenta which underlie the feto-placental growth retardation associated with exposure to polyromatic hydrocarbons (PAH) during pregnancy. The first specific aim will investigate whether exposure of human placental cells to benzo(a)pyrene (BP) and related PAH compounds alters the differentiation to trophoblast cells. Experiments are proposed to quantitate the effects of BP on cytotrophoblast fusion to form syncytia and on the expression of the biochemical markers of differentiation, chorionic gonadotrophin (hCG), placental lactogen (hPL), and pregnancy-specific B1 glycoprotein (hPSBG). The effects of BP on EGF receptors will be examined to determine if down-regulation of receptors is correlated temporally with changes in differentiation state. The second specific aim will examine rat placenta to determine whether exposure to prototype PAH compounds alters growth factor production or receptor function at the maternal-fetal interface. Studies will determine whether BP, B-naphthoflavone (BNF) 3-methylcholanthrene, (3MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) have direct effects on trophoblast cells, or whether trophoblast cells are altered indirectly by changes in cytokine production from maternal decidua. The final specific aim is to evaluate whether cytokines, particularly IL-1, modulate the induction of cytochrome P-450IA1 in placental cells.