Manchester D K, Parker N B, Bowman C M
Pediatr Res. 1984 Nov;18(11):1071-5. doi: 10.1203/00006450-198411000-00002.
It is unclear whether placental xenobiotic metabolism can protect the human conceptus. In particular, the role of placental metabolism of toxic components of cigarette smoke such as polycyclic aromatic hydrocarbons (PAHs) is poorly understood. We hypothesized that increased aryl hydrocarbon hydroxylase (AHH) activity observed in placentas from smokers might help clear PAHs from maternal circulation and thereby prevent transplacental induction of AHH by PAHs. Our studies of AHH activity in human placentas and umbilical vein endothelium support this premise. While AHH activity was significantly increased in placentas from smokers compared with activity in placentas from nonsmokers, AHH activity in umbilical vein endothelium from these same pregnancies was unaffected by maternal smoking and remained low. In order to confirm that AHH present in endothelium was inducible, we also demonstrated dose-dependent increases in AHH activity in primary cultures of human umbilical vein endothelial cells exposed to PAHs. These findings may indicate first pass protection of the fetus by placental xenobiotic metabolism, or that endogenous factors suppress AHH induction in the fetus but not placenta.
尚不清楚胎盘的外源性物质代谢是否能保护人类胚胎。尤其是，胎盘对香烟烟雾中多环芳烃（PAHs）等有毒成分的代谢作用还知之甚少。我们推测，吸烟者胎盘中观察到的芳烃羟化酶（AHH）活性增加可能有助于清除母体循环中的PAHs，从而防止PAHs经胎盘诱导AHH。我们对人胎盘和脐静脉内皮中AHH活性的研究支持这一假设。与非吸烟者的胎盘相比，吸烟者胎盘的AHH活性显著增加，但同一孕期脐静脉内皮中的AHH活性不受母体吸烟影响，仍保持在较低水平。为了证实内皮中的AHH是可诱导的，我们还证明了暴露于PAHs的人脐静脉内皮细胞原代培养物中AHH活性呈剂量依赖性增加。这些发现可能表明胎盘外源性物质代谢对胎儿有首过保护作用，或者内源性因素抑制胎儿而非胎盘的AHH诱导。
