ABSTRACT
The effects of repeated prenatal stress with different severity (restraint and immobilization) on Fos expression in the maternal and fetal hypothalamic paraventricular nucleus (PVN) were examined in rats. Acute stress treatment was performed for 30 min on gestational day 21, and repeated stress treatment for 30 min daily for 5 days from gestational days 17-21. In the parvocellular region of the maternal PVN, the stress-induced increases in the number of Fos-immunoreactive neurons were smaller in the repeated stress groups than the acute stress groups, indicating an adaptation of Fos expression to repeated stress. The attenuated Fos expression observed in the maternal PVN following repeated mild stress did not occur in the fetal PVN. In contrast, repeated immobilization stress caused a much smaller increase in Fos expression in the fetal PVN than did acute immobilization stress. The reduced Fos expression in the fetal PVN following repeated severe stress was thought to be due to cell death, since the fetal PVN in the chronic immobilization group revealed a reduction in the total number of cells and an increase in the number of apoptotic cells. In the female but not male fetuses, repeated restraint stress induced a significant increase in the number of apoptotic cells in the PVN. These findings suggest that the fetal PVN shows no adaptation of Fos expression to repeated maternal stress, but great vulnerability to cell death, including apoptosis. In addition, stress-induced apoptosis may more easily occur in the fetal PVN in females than males.
Subject(s)
Paraventricular Hypothalamic Nucleus/embryology , Pregnancy Complications/psychology , Prenatal Exposure Delayed Effects , Stress, Psychological , Acute Disease , Animals , Body Weight , Chronic Disease , Disease Models, Animal , Female , Fetus/physiology , Gestational Age , Male , Paraventricular Hypothalamic Nucleus/physiopathology , Pregnancy , Rats , Rats, Sprague-Dawley , Restraint, Physical , Sex CharacteristicsSubject(s)
Amphotericin B/administration & dosage , Leukemia, Myeloid, Acute/complications , Liver Abscess/drug therapy , Adult , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Cytarabine/administration & dosage , Cytarabine/analogs & derivatives , Daunorubicin/administration & dosage , Humans , Leukemia, Myeloid, Acute/drug therapy , Liver Abscess/etiology , Male , Mercaptopurine/administration & dosage , Portal System , Prednisolone/administration & dosageABSTRACT
Experiments with rat liver homogenates showed that on subcellular fractionation the ability to catalyse the conversion of thyroxine into tri-iodothyronine was lost. The activity could in part be restored by addition of the cytosol to the microsomal fraction. Both components were found to be heat labile. The necessity of the presence of cytosol could be circumvented by incorporation of thiol-group-containing compounds in the medium. Optimal enzymic activity was observed in the presence of dithiothreitol and EDTA in medium of low osmolarity. By comparing the distribution of the converting enzyme over the subcellular fractions with a microsomal marker enzyme, glucose 6-phosphatase, it was demonstrated that the former is indeed of microsomal origin. Finally, it was shown that thiol groups play an essential role in the conversion of thyroxine into tri-iodothyronine.
