Oxidative stress parameters in plasma of Huntington's disease patients, asymptomatic Huntington's disease gene carriers and healthy subjects : A crosssectional study. Journal of Neurology, 254 (12). pp. 1676-1683.

No abstract

Glycogen deposition was determined in pregnant rats and their fetuses twenty four hrs after maternal treatment with dexamethasone in the final days of pregnancy. Dexamethasone increases glycogen accumulation in the fetal liver, heart, adrenal glands and thymus. Simultaneously, it increases the glycogen concentration in maternal liver. In this study, dexamethasone did not change the glycogen level in the fetal kidneys, brain, placenta, lung and maternal adrenal glands. These results show that dexamethasone accelerated glycogen deposition in some fetal tissues. It is possible that dexamethasone activated enzymes of glycogen synthesis or potentiated the action of fetal corticosterone on induction of glycogen accumulation in fetal rat tissues.

No abstract

Pregnant rats were treated with dexamethasone in drinking water (10 micrograms/ml) from the 15th to the 22nd day of pregnancy. Dexamethasone significantly depressed cell numbers in fetal rat adrenal glands, liver, lung, testes and pituitary from the 17th to the 22nd day of pregnancy. These data indicated that dexamethasone retarded cell multiplication in rat fetuses. Weight per cell and protein per cell were less in fetal adrenal glands, kidneys and pituitary after treatment with dexamethasone. Dexamethasone had no effect on RNA per cell in various fetal tissues. The nucleic acid synthesis in vitro from 3H-thymidine and 3H-uridine were reduced in all observed fetal tissues after dexamethasone treatment on the 22nd day of pregnancy. These results show that dexamethasone has a multisystemic effect on fetal rat development, depressing nucleic acid synthesis and depleting cell numbers and cell size in various fetal tissues.