Influence of maternal dietary zinc intake on in vitro tubulin polymerization in fetal rat brain

The hypothesis that one of the biochemical lesions underlying zinc deficiency-induced teratogenicity is altered microtubule formation was tested. Day 19 fetuses from zinc-deficient Sprague-Dawley dams were characterized by low brain supernate zinc concentrations and slow brain tubulin polymerization rates compared to controls. Brain supernate tubulin and protein concentrations were similar in zinc-deficient and control fetuses. In vitro brain tubulin polymerization rates were increased following addition of zinc to either control or zinc-deficient brain supernates; however, the stimulatory effect of added zinc on polymerization was significantly higher in brain supernates obtained from zinc-deficient fetuses compared to controls. These results support the idea that one effect of fetal zinc deficiency is a reduction in tubulin polymerization, which in turn may result in altered microtubule function.     

Co-existence of renin-like immunoreactivity in the rat maternal and fetal neocortex

Renin-like immunoreactive material was examined in maternal and fetal brain. A continuous layer of renin was localized in neocortex which begins in the fetal brain during gestation and continues throughout the animal's normal life.     

ACTH and growth hormone relationship in fetal rat adrenal steroidogenesis in vitro.

The effects of growth hormone and ACTH, alone or in combination, on fetal rat adrenal steroidogenesis in vitro were examined on the last day of intrauterine development. ACTH increased, while growth hormone did not affect fetal adrenal weight. ACTH increased fetal rat adrenal steroidogenesis, hydroxylation of 4-14C-progesterone to corticosterone, 18-hydroxy-11-deoxycorticosterone, 11-hydroxycorticosterone and aldosterone. Growth hormone alone had no effect on fetal adrenal steroidogenesis. ACTH and growth hormone administered together increased the conversion of progesterone to the above mentioned steroids to a greater extent than ACTH alone. The results indicate that growth hormone may participate in the fetal rat adrenal steroidogenesis potentiating the effects of fetal pituitary ACTH.     

Morphological alterations in the developing fetal rat limb due to maternal injection of chlorambucil

On day 14 of pregnancy, rats were injected i.p. with 9.5 mg/kg of chlorambucil. At term, all the fetuses were stunted and had obvious skeletal malformations. From days 15-20 of gestation there was a steady progression of cell death and histologic derangement in long bone formation. This began on day 15, the day following exposure to chlorambucil, with extensive cell death of chondroblasts in the long bone primordia. By day 16, dead or dying cells were located in the cartilage model and became associated with a higher than normal matrix to cell ratio. In day 17 limbs, many cells of the cartilage model were irregular in size and shape so that the normally precise cellular arrangement was lacking. On day 18, periosteal and enchondrial calcification was delayed and scanty. The fibular hemimelia observed in all drug-treated term fetuses stained with alizarin appeared to result from lack of development of the proximal half of the cartilage model. The observed alterations, particularly bowing of the ulna, in the teratogen-treated fetuses appeared to result primarily from specific cell death and formation of aberrant cell types but abnormal cell products may also play a role.     

Effects of insulin and maternal diabetes on fetal lipogenesis in the rat

Offspring of diabetic mothers have been investigated with regard to fetal hepatic and brown adipose tissue lipogenesis in the rat. Results, which cannot be explained by existing theory, are obtained from offspring of subdiabetic mothers and manifest diabetic mothers. In re-evaluating the effect of exogenous insulin on perinatal lipogenesis, we find important differences in hormone sensitivity between liver and brown adipose tissue.     

The relationship of conceptus number and fetal sex to maternal serum testosterone concentration in the rat

On Day 8 of pregnancy, the number of implantation sites in pregnant rats was adjusted to 1, 2, 4, 6, or greater than 10. Blood was collected on Days 11, 12, 15, 18, and 20 for the determination of serum testosterone, progesterone, and androstenedione. Serum testosterone levels exhibited a direct linear relationship with implantation number, increasing from 1 through greater than 10 implants. This linear relationship was particularly evident at Days 12, 15, and 18 of pregnancy. Serum progesterone levels increased from one to four conceptuses and plateaued above this number. There was no apparent relationship between the number of conceptuses and serum androstenedione levels, which may reflect the multiple origins of this steroid in the pregnant rat. In a separate group of rats in which the number of conceptuses was adjusted to three on Day 8 of pregnancy, blood was collected on Days 11, 12, 15, 18, and 20. Fetal sex was determined between the last bleeding and the day of parturition. Serum testosterone was determined and results were examined with regard to the number of male/female fetuses in the litter of three. There was no relationship between maternal serum testosterone levels and the number of male fetuses, indicating that the fetal testis does not make a significant contribution to circulating maternal testosterone levels.     

Collagen degradation in ischaemic rat hearts.

Myocardial extracellular matrix is organized into a complex arrangement of intercellular and pericellular fibres and fibrils that serves as a supporting framework for contracting cells. Recent evidence suggests that changes in ventricular shape and function occurring after ischaemic injury may be related to alterations of this matrix. In this report we describe the rapid and extensive loss of collagen in myocardial infarction produced by ligating the left anterior descending coronary artery of the rat for 1-3 h. The total collagen content in the myocardial infarct zones after 1, 2 and 3 h of ligation was 75 +/- 8%, 65 +/- 7% and 50 +/- 10% respectively (mean +/- S.D.) of that of either the non-infarcted tissue controls or of the same regions in sex- and age-matched normal left ventricles. A marked decrease also occurred in the residual collagens which were not extractable with 6 M-guanidine hydrochloride, suggesting that rapid degradation of insoluble collagen fibres may also occur. The decreased collagen content in the 3 h myocardial infarct coincided with the appearance of several enzyme activities. Collagenase, other neutral proteinase and presumed lysosomal serine proteinase activities were increased by 3, 3 and 2 times the control values respectively. These results suggest that the increased activities of collagenase and other neutral proteinases may be responsible for the rapid degradation of extracellular matrix collagen in myocardial infarct.     

Development in vitro of epithelial-cell monolayers derived from fetal rat pancreas.

Purified epithelial-cell monolayers were generated in vitro from explants of fetal rat pancreas. The extent of the development of the epithelial monolayer, as determined by planimetric analysis, was enhanced by the application of two methodological procedures: (a) preincubation of fetal pancreas in situ at 27 degrees C for 5 hr prior to dissection and explantation; and (b) incubation of the explants in medium containing a high concentration (50% to 70%) of fetal bovine serum. By utilizing such culture conditions, sheets of contiguous epithelial cells, with little or no peripheral fibroblastic contamination, were maintained for 9 days. Whereas the majority of cells within the monolayer had morphological characteristics of pancreatic ductal cells, endocrine cells were identified by the specific immunocytochemical localization of insulin and glucagon. In addition, insulin could be detected in the incubation medium throughout the course of experiment. The simplicity of this preparation offers some advantages over other techniques including reduced chance of contamination and reduced cellular damage or death. It provides a model for future studies directed toward developing individual cell strains derived from pancreatic epithelial cells.     

Micronucleus formation in fetal maternal rat erythroblasts after norfloxacin transplacental administration

Single oral doses of norfloxacin (4, 2, 1, 0.5 mmole/kg) administered to pregnant rats significantly increase the frequency of micronucleated polychromatic erythrocytes both in fetal liver and in maternal bone marrow. Therefore norfloxacin in this work has been found to be a genotoxic agent.     

Cellular immune aspects of the human fetal maternal relationship. II. In vitro response of gravida lymphocytes to phytohemagglutinin

At optimal doses of phytohemagglutinin, human gravida lymphocytes showed no depression of responses when compared to nonpregnant female control lymphocytes. Compared to the control cells, gravida lymphocytes also seemed to have a higher spontaneous incorporation, a higher response at suboptimal PHA concentrations, and a lower peak dose response. These findings were more evident in the latter third of the pregnancy and suggest that maternal lymphocytes by this test are apparently fully reactive, and that they are undergoing low-level stimulation.     

Human maternal and fetal response to graded exercise

Six healthy active women in the third trimester of pregnancy participated in a graded exercise protocol to levels of exertion perceived to be equivalent to that of their usual exercise regimen. Fetal heart rate response (FHR) was documented by ultrasound transducer and confirmed (n = 1) by ultrasonic visualization. Resting maternal O2 consumption was 277 +/- 50 (SD) ml/min and rose to 1,132 +/- 202 ml/min at a mean final exercise intensity of 79 +/- 9 W after 12.8 +/- 1.7 min on a cycle ergometer. There was no significant change in maternal serum insulin, growth hormone, glucose, or pH values. Maternal leukocyte count, hemoglobin, and venous lactate levels rose significantly during the exercise (P less than 0.05). FHR prior to exercise was 142 +/- 4 beats/min and decreased to 84 +/- 34 beats/min during exercise. The decrease in FHR was documented within 1 min of initiating exercise in all cases. During exercise, fetal movements were not accompanied by FHR accelerations. Within 1 min following the cessation of exercise, FHR rose to 143 +/- 8 beats/min and fetal movements were accompanied by FHR accelerations. Since the recovery of FHR occurred immediately after cessation of maternal exercise, this level of maternal exercise does not appear to be harmful to the fetus.