A Study on Correlation of Vascular Endothelial Growth Factor in Preeclampsia / 대한주산의학회잡지

OBJECTIVE: The purpose of this study was to assess the impact of vascular endothelial growth factor (VEGF) in pregnancies with mild and severe preeclampsia. METHODS: From January 1999 to June 2001, we studied the severity for pregnant women with pregnancy induced hypertension between 28 and 40 weeks gestation. In the mild (n=46) and severe preeclamptic women (n=28), the laboratory evaluation included liver function test, platelet counts, and serum creatinine. The systolic/diastolic (S/D) ratio of the fetal umbilical artery flow for placental resistance was measured by ultrasonographic doppler velocimetry. To detect the damage of vascular endothelial cells in all preeclamptic women, serum concentrations of VEGF were measured. RESULTS: Severe preeclampsia had more elevated liver enzymes, thrombocytopenia, high creatinine than mild preeclampsia. HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) was encountered in 8/28 (28.6%) of severe preeclampsia. Fifteen out of twenty-eight cases (53.6%) in severe preeclampsia had elevated S/D ratio from 3.0 to 4.5 including 6 cases with absent end diastolic velocity, whereas 4/46 (8.7%) was elevated SD ratio (>3.0) in mild preeclampsia. Serum concentrations of VEGF were elevated in both mild (7.5+/-4.9 ng/mL, p<0.05) and severe preeclampsia (19.3+/-8.8 ng/mL, p<0.05) compared to normal pregnancy (0.5~2.1 ng/mL). CONCLUSION: The higher serum concentration of VEGF and elevated S/D ratio of umbilical artery were responsible for the changes of the resistance of placental blood flow in severe preeclampsia. Furthermore, elevated S/D ratio of umbilical artery velocity was essential as a surveillance method of fetal health status with IUGR (Intrauterine growth restriction) by vascular declination of placenta.

Involvement of Oxidative Stress in Cisplatin-Induced Apoptosis in HeLa Cells / 대한산부인과학회잡지

OBJECTIVE: To determine whether oxidants are formed as part of the cisplatin-induced apoptotic process, intracellular markers of oxidative stress were examined. METHODS: Apoptotic death of HeLa cells by cisplatin was confirmed by flow cytometry. RESULTS: The pre-treatment with glutathione (GSH) significantly attenuated cisplatin-induced apoptosis through the reduction of reactive oxygen species (ROS) accumulation and diminished caspases-3 and 9 protease activity. Furthermore, z-VAD-fmk, an inhibitor of pan-caspase, effectively inhibited the activation of caspases and prevented apoptosis by cisplatin, although cisplatin-induced ROS generation was not attenuated. CONCLUSION: These data indicate that ROS may play a role as an upstream mediator of caspases. Taken together, our results suggest that oxidative stress mediates cisplatin-induced apoptosis in HeLa cells.