growth restriction triggered by polycyclic aromatic hydrocarbons is associated with altered placental vasculature and AhR-dependent changes in cell death.

The high miscarriage rates observed in women smokers raises the possibility that chemicals in cigarette smoke could be detrimental to embryo development. Previous studies have established that polycyclic aromatic hydrocarbons (PAHs), transactivate the arylhydrocarbon receptor (AhR), leading to cell death. Herein we show that PAH exposure results in murine embryo cell death, acting as a potential mechanism underlying cigarette-smoking-induced pregnancy loss. Cell death was preceded by increases in Bax levels, activation of caspase-3 and decreased litter size. Chronic exposure of females to PAHs prior to conception impaired development, resulting in a higher number of resorptions. This embryonic loss could not be prevented by the disruption of Hrk, but was diminished in embryos lacking Bax. We conclude that exposure of early embryos to PAHs reduces the allocation of cells to the embryonic and placental lineages by inducing apoptosis in a Bax-dependent manner, thus compromising the developmental potential of exposed embryos.

Objective: The objective of this study was to explore whether increased levels of granulocyte elastase in cervical secretion is an independent predictive factor for preterm delivery before 34 weeks of gestation in the patient with preterm labor. Methods: One hundred and sixty-one women with preterm labor at 22–28 weeks of gestation were enrolled prospectively. The level of granulocyte elastase in cervical secretions was measured by immunoassay, vaginal secretions were collected for the microscopic evaluation of Gram-stained smears, and the uterine cervix was assessed by transvaginal ultrasonography. Results: Nineteen of 161 patients (12%) delivered before 34 weeks of gestation. Granulocyte elastase assessment had a sensitivity, specificity, positive predictive value, and negative predictive value for preterm delivery of 53, 75, 22 and 92%, respectively. A positive elastase assessment was associated with a relative risk for preterm delivery of 2.9 (95% CI 1.3–6.6), whereas a positive bacterial vaginosis assessment and shorter cervical length less than 25 mm demonstrated a relative risk of 1.9 (95% CI 0.8–4.6) and 1.5 (95% CI 0.6–5.0), respectively. Conclusion: The present study demonstrates that the risk of spontaneous preterm delivery before 34 weeks of gestation is increased in the women with preterm labor who are found to have an increased level of granulocyte elastase in cervical secretions.

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The objective of the present study was to explore whether a free radical spin trap agent, alpha-phenyl-N-tert-butyl nitrone (PBN), influences bioenergetic failure induced in the 20-day-old fetal brain by 30 min of intrauterine ischemia in Wistar rats. Fetal brains were frozen in situ at the end of ischemia and after 1, 2, and 4 h of recirculation for analysis of ATP, ADP, AMP, and lactate. PBN or vehicle was given 1 h after recirculation. Tissue oxygen tension was evaluated in placental and fetal cerebral tissues throughout the whole periods of 30 min of ischemia and 4 h of recirculation. Ischemia was associated with a decrease in ATP concentration and an increase in lactate concentration (p < 0.001). Recirculation (1 and 2 h) led to a recovery of ATP concentration, but continued reflow (4 h) was associated with a secondary deterioration of high-energy phosphates (p < 0.01). Lactate concentration increased during this recovery period. This deterioration was prevented by PBN (p < 0.05). After 30 min of ischemia, tissue oxygen tension in placenta and fetal brain decreased to about 30% and 50% of control, respectively. However, recirculation brought about a recovery of oxygen delivery. The results indicate that although during the early time period after ischemia fetal cerebral energy metabolism is maintained by an acceleration of the anaerobic glycolytic rate, secondary deterioration of cellular bioenergetic state develops in the immature fetal brain. This deterioration may be due to mitochondrial dysfunction, which may be induced by oxygen-derived free radicals, and not by compromised microcirculation.

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