A study was undertaken to 1) determine the effects of tobacco smoke exposure on maternal and neonatal weight and body mass index (BMI) and placental weight, volume and surface area and 2) establish any correlations between the placental surface area, volume and weight with maternal and neonatal body weight and BMI in mothers exposed to cigarette smoke. A total of 154 full-term placentae, 65 from mothers exposed to tobacco smoke and 89 from non-exposed mothers were collected from Kuala Lumpur Maternity Hospital. The placental surface area was determined using a stereological grid, the volume by Scherle's method and the weight by using an electronic weighing machine. In general there were no differences in maternal, placental and neonatal parameters between the exposed and non-exposed groups. However, there were significant correlations between placental weight with maternal weight and maternal BMI in both exposed (r = 0.315; p = 0.013) and (r = 0.265; p = 0.038), and non-exposed (r = 0.224; p = 0.035) and (r = 0.241; p = 0.023) mothers. It was also found that the maternal weight on admission correlated significantly with placental weight in both Malay (r = 0.405; p = 0.020) and Indian (r = 0.553; p = 0.050) passive smokers. Correcting the placental parameters for the maternal weight had no effect on the results.
Many plant-derived natural compounds have been reported previously to inhibit the production of important pro-inflammatory mediators such as nitric oxide, prostaglandin E2, TNF-alpha and reactive oxygen species by suppressing inducible enzyme expression via inhibition of the mitogen-activated protein kinase pathway and nuclear translocation of critical transcription factors. This study evaluates the effects of atrovirinone [2-(1-methoxycarbonyl-4,6-dihydroxyphenoxy)-3-methoxy-5,6-di-(3-methyl-2-butenyl)-1,4-benzoquinone)], a benzoquinone that we have previously isolated from Garcinia atroviridis, on two cellular systems that are repeatedly used in the analysis of anti-inflammatory bioactive compounds, namely, RAW 264.7 macrophage cells and whole blood. Atrovirinone inhibited the production of both nitric oxide and prostaglandin E2 from LPS-induced and IFN-gamma-induced RAW 264.7 cells and whole blood, with inhibitory concentration (IC)50 values of 4.62 +/- 0.65 and 9.33 +/- 1.47 micromol/L, respectively. Analysis of thromboxane B2 (TXB2) secretion from whole blood stimulated by either the cyclooxygenase (COX)-1 or the COX-2 pathway showed that atrovirinone inhibits the generation of TXB2 by both pathways, with IC50 values of 7.41 +/- 0.92 and 2.10 +/- 0.48 micromol/L, respectively. Analysis of IC50 ratios showed that atrovirinone was more COX-2 selective in its inhibition of TXB2, with a ratio of 0.32. Atrovirinone also inhibited the generation of intracellular reactive oxygen species and the secretion of TNF-alpha from RAW 264.7 cells in a dose-responsive manner, with IC50 values of 5.99 +/- 0.62 and 11.56 +/- 0.04 micromol/L, respectively. Lipoxygenase activity was also moderately inhibited by atrovirinone. Our results suggest that atrovirinone acts on important pro-inflammatory mediators possibly by the inhibition of the nuclear factor-kappaB pathway and also by the inhibition of the COX/lipoxygenase enzyme activity.