Ubiquinol-10 and ubiquinone-10 levels in umbilical cord blood of healthy foetuses and the venous blood of their mothers.

Despite their being good markers of oxidative stress for clinical use, little is known about ubiquinol-10 (reduced coenzyme Q10) and ubiquinone-10 (oxidized coenzyme Q10) levels in foetuses and their mothers. This study investigates oxidative stress in 10 healthy maternal venous, umbilical arterial and venous bloods after vaginal delivery by measuring ubiquinol-10 and ubiquinone-10 levels. Serum ubiquinol-10 and ubiquinone-10 levels were measured by HPLC with a highly sensitive electrochemical detector. Maternal venous ubiquinol-10 and ubiquinone-10 levels were significantly higher than umbilical arterial and venous levels (all p < 0.001). However, the ubiquinone-10/total coenzyme Q10 (CoQ10) ratio, which reflects the redox status, was significantly higher in umbilical arterial and umbilical venous blood compared to maternal venous blood (all p < 0.001). The ubiquinone-10/total CoQ10 ratio was higher in umbilical arterial than in umbilical venous blood (p < 0.01). The present study demonstrated that foetuses were under higher oxidative stress than their mothers.

Positive correlation between maternal serum coenzyme Q10 levels and infant birth weight.

The purpose of this study was to examine the relationship between the level of maternal serum coenzyme Q10 (CoQ10), which is a lipid-soluble antioxidant, maternal body weight gain, fat mass gain, and infant birth weight. A longitudinal observational study was conducted with 50 healthy pregnant women (average age: 31.1 years, average body mass index (BMI): 21.3 kg/m(2) at prepregnancy) at each trimester. CoQ10 levels were measured by high performance liquid chromatography. Maternal weight and body composition were measured by a bioelectrical impedance analysis. The CoQ10 levels significantly increased throughout pregnancy from the first trimester to the third trimester (P < 0.001), and correlated with not only the serum cholesterol levels (P < 0.01) but also with the serum acetoacetic acid levels (P < 0.05) in the third trimester. The CoQ10 levels correlated with the maternal weight gain (P < 0.05) and fat mass gain (P < 0.05) from the second to the third trimester, after adjusting for lipid markers, age, and smoking habits. The level of CoQ10 during the third trimester was also significantly associated with the infant birth weight (P < 0.05) after adjusting for gestational age, maternal prepregnancy BMI, and smoking habits. Therefore, it is concluded that the level of maternal CoQ10 is positively associated with fetal growth, balancing rapid metabolic changes in the last half of a normal pregnancy.

Gastric estrogen directly induces ghrelin expression and production in the rat stomach.

Ghrelin, an endogenous ligand for the GH secretagogue receptor, is predominantly produced in the stomach. Little is known about the regulation mechanism of gastric ghrelin. Here, we report that estrogen synthesized in the stomach induces rat gastric ghrelin gene expression and production. We established a gastric ghrelin cell enrichment method using Percoll centrifugation and then studied the effect of estrogen and/or its antagonist on ghrelin expression and production. Treatment with estrogen for 8 h significantly increased the level of ghrelin expression, and ICI-182 780, an estrogen receptor (ER) antagonist, completely reversed this effect. Reverse transcriptase-PCR analysis clearly showed that ERalpha and aromatase are expressed in the female rat stomach. Moreover, treatment with an aromatase inhibitor, 4-hydro-xyandrostenedione (formestane), significantly decreased the level of ghrelin mRNA expression in minced stomach tissue. In vivo studies revealed that the ghrelin mRNA expression and production did not change in gonadectomized rat 3 weeks after surgery. These results strongly suggest that estrogen produced in the stomach directly induces ghrelin expression and production in both female and male rat stomachs.