Ng Sheung P, Steinetz Bernard G, Lasano Salamia G, Zelikoff Judith T
New York University School of Medicine, Nelson Institute of Environmental Medicine, Tuxedo, NY, USA.
Exp Biol Med (Maywood). 2006 Sep;231(8):1403-9. doi: 10.1177/153537020623100814.
Epidemiologic evidence indicates that maternal smoking increases the risk of preterm birth. While a number of plausible mechanisms for early delivery have been offered, the role of gestational hormones in this smoke-induced outcome is uncertain. Thus, a toxicologic study was performed to examine the effects and underlying hormonal mechanisms of mainstream cigarette smoke (MCS) exposure on gestational duration. Pregnant B6C3F1 mice were exposed by inhalation to MCS for 5 days/week (4 hrs/day) from Gestational Day (GD) 4 to parturition. Smoke-induced effects on gestational length, interpubic ligament length, maternal hormone secretion patterns (estradiol-17beta, progesterone, prolactin, and relaxin), body weight gain, postimplantation loss, litter size, and offspring sex ratio were examined. Dams exposed to MCS at a concentration equivalent to smoking less than one pack of cigarettes/day (carbon monoxide = 25 parts per million, total suspended particulates = 16 mg/m3) demonstrated a significant (P < 0.05) shortening of gestational duration (compared with pregnant, air-exposed mice). In addition, MCS-exposed mice sacrificed on GD 18 had significantly (P < 0.05) increased interpubic ligament length, elevated serum estrogen levels, and a reduced progesterone to estradiol-17beta ratio (compared with air-exposed controls); levels of progesterone and prolactin were only modestly decreased and increased, respectively, in the MCS-exposed mice. Smoke exposure had no significant effects on maternal relaxin levels, body weight gain, postimplantation loss, litter size, or sex ratio. Results of this study demonstrate that inhalation exposure of pregnant mice to a low dose of MCS shortens gestation and alters hormone secretory patterns, which are important for maintaining pregnancy and inducing parturition. These findings support the view that pregnant women who smoke (even modestly) may be at increased risk for preterm birth, and that early delivery may be related (at least partly) to MCS-induced.
流行病学证据表明，孕妇吸烟会增加早产风险。虽然已经提出了一些关于早产的合理机制，但妊娠激素在这种烟雾诱导的结果中的作用尚不确定。因此，进行了一项毒理学研究，以检查主流香烟烟雾（MCS）暴露对妊娠期的影响及其潜在的激素机制。将怀孕的B6C3F1小鼠从妊娠第4天至分娩期间，每周5天（每天4小时）通过吸入暴露于MCS。研究了烟雾对妊娠期长度、耻骨间韧带长度、母体激素分泌模式（雌二醇-17β、孕酮、催乳素和松弛素）、体重增加、着床后丢失、窝仔数和后代性别比例的影响。暴露于相当于每天吸烟少于一包香烟浓度的MCS的母鼠（一氧化碳 = 百万分之25，总悬浮颗粒物 = 16毫克/立方米）妊娠期显著缩短（P < 0.05）（与暴露于空气的怀孕小鼠相比）。此外，在妊娠第18天处死的暴露于MCS的小鼠耻骨间韧带长度显著增加（P < 0.05），血清雌激素水平升高，孕酮与雌二醇-17β的比值降低（与暴露于空气的对照组相比）；暴露于MCS的小鼠中，孕酮和催乳素水平仅分别适度降低和升高。烟雾暴露对母体松弛素水平、体重增加、着床后丢失、窝仔数或性别比例没有显著影响。这项研究的结果表明，怀孕小鼠吸入低剂量的MCS会缩短妊娠期并改变激素分泌模式，而这些对于维持妊娠和诱导分娩很重要。这些发现支持这样一种观点，即吸烟的孕妇（即使是少量吸烟）可能早产风险增加，并且早产可能（至少部分）与MCS诱导有关。
