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At least 55 records · Page 3Linked to original sources
PubMed1993

Genital and nongenital teratogenesis of prenatal progestogen therapy: the effects of 17 alpha-hydroxyprogesterone caproate on embryonic and fetal development and endochondral ossification in the C57B1/6J mouse.

OBJECTIVE: The current study assesses the effects of 17 alpha-hydroxyprogesterone caproate on embryo-fetal development, with a particular focus placed on intrauterine endochondral bone development and growth. STUDY DESIGN: Primigravid C57 BI/6J mice were administered 17 alpha-hydroxyprogesterone caproate by means of subdermal pellets designed to deliver doses of 0.5, 5.0, and 50.0 mg/kg/day on gestational days 7 through 19. Assuming a dosage regimen of 250 mg per 50 kg per week in humans for the treatment of threatened spontaneous abortion, the doses used were 0.7, 7.0, and 70.0 times the human dose equivalent. The time course of exposure encompassed the period of organogenesis through the late fetal period. RESULTS: No maternal toxicity was noted throughout the course of 17 alpha-hydroxyprogesterone caproate administration. Fetal weight at term and the percentage of resorptions, dead fetuses, male fetuses, and malformations at term were not significantly affected at any evaluated dose when compared with control group values. The steroid did not exert a significant influence on any assessed parameter of endochondral bone development or growth, even at a dosage concentration that far exceeded the human therapeutic dose equivalent. As would be expected, fetal weight was directly correlated with diaphyseal length and also influenced the relationship of cartilage to osseous tissue in both the humeri and femora. There were no 17 alpha-hydroxyprogesterone caproate dose and fetal sexual phenotype interactive effects noted with regard to any developmental or bone growth parameter measured, thus discounting any sexual phenotype-related toxic or teratogenic sensitivities. CONCLUSION: The data indicate that 17 alpha-hydroxyprogesterone caproate administered at doses of up to 70 times the human dose equivalent did not induce increases in the frequency of genital and, importantly, nongenital teratogenesis in spite of exposure during the critical period of organogenesis. Additionally, the steroid did not affect limb morphogenesis or endochondral ossification.

17 alpha-Hydroxyprogesterone Caproate↗
PubMed1997

Embryonic and fetal development in different genotypes in pigs.

It is widely accepted that uterine capacity, not ovulation rate, is the greatest restraint on litter size in pigs. Recently, the reproductive strategy(s) of the Chinese Meishan pig, a breed which farrows three to five more piglets per litter than US or European pig breeds, has come under intense scrutiny. It was initially determined that the Meishan female could farrow more viable piglets per litter than US or European pig breeds, with a uterine size and ovulation rate equivalent to those of less prolific breeds. It has become apparent that the Meishan conceptus exhibits a reduced trophectoderm mitotic rate during the preimplantation period, elongates from fewer cells and remains smaller throughout gestation compared with conceptuses from less prolific US or European pig breeds. This strategy by the Meishan conceptus for a lower growth rate results in a marked reduction in conceptus loss through day 18 of gestation compared with less prolific breeds. An additional strategy is required in the Meishan to allow the larger number of viable fetuses to survive after day 30 of gestation when uterine capacity becomes limiting. Our research has demonstrated that the rapid growth of the fetus in US pig breeds appears to require continued placental growth to increase the surface area for nutrient exchange. In contrast, the increased number of smaller Meishan fetuses achieve the same increase in placental efficiency by markedly increasing the density of placental blood vessels at the fetal-maternal interface. This proliferation of placental blood vessels obviates the need for marked increase in placental size.

Animals↗
PubMed2002

Effects of chlorophyllin on mouse embryonic and fetal development in vivo.

Chlorophyllin (CHL) has proven that there is antimutagenic and anticarcinogenic activity in several organisms without causing lethal effects. However, there is no information about its effects when it is administered in gestation. In the present study, we assessed possible effects of CHL when it was administered to CD-1 mice on the 8th day of gestation using the same doses and administration route used in ours previous antimutagenic and antigenotoxic studies. Females were exposed to a single dose of CHL by i.p. injection (20, 40, 50, or 100mg/kg b.w.). On day 18 all dams were subjected to cesarean section and the fetuses were examined with common teratological methods. Results show that CHL-treatment induced total litter loss and is dose-dependent, probably due to either the interaction between CHL and some general control mechanisms of embryo development or by an impairment of maternal-fetal interactions. The analysis of uterine horns of the CHL-treated females with total litter loss revealed the presence of green rings in the uterus. Results show the inverse relationship between the number of live implants and the frequency of green rings, indicating implantation sites where embryo death and early resorptions occurred. Although CHL was given in a single dose on day 8 in this study, the results indicate that CHL is associated with significant embryo lethality.

Animals↗
PubMed1985

Abnormal embryonic development induced by antibodies to rat visceral yolk-sac endoderm: isolation of the antigen and localization to microvillar membrane.

An antigenic substance was isolated from rat visceral yolk-sac endoderm of the 18th-20th days of gestation by extraction with the nonionic detergent Nonidet P-40, Sephacryl S-300 gel filtration, and Ricinus communis agglutinin affinity chromatography. The rabbit antiserum directed against this antigenic substance when injected into pregnant rats during the period of organogenesis caused abnormal embryonic development, fetal growth retardation, and embryonic death. Ouchterlony gel diffusion analysis demonstrated that the antiserum formed one immunoprecipitin band against the crude detergent extract and a complete identity between the present visceral yolk-sac antigen and the renal glycoprotein antigen previously isolated (C. C. K. Leung, (1982) J. Exp. Med. 156, 372-384). The antigen eluted from the antibody affinity column appeared to consist of two major peptides of 60 and 30 kDa when analyzed by SDS-polyacrylamide gel electrophoresis. Indirect immunofluorescent and immunoperoxidase localization studies at the light microscopic level demonstrated that both rat renal proximal tubule and embryonic visceral yolk-sac endoderm at various gestational stages (including the organogenetic period) shared the same antigen. Indirect immunoperoxidase localization studies at the electron microscopic level demonstrated that the antigen was a part of (or associated with) the microvillar membrane and membrane invaginations at the base of the microvilli of the renal proximal tubule and visceral yolk-sac endoderm. In vivo immunoperoxidase localization studies demonstrated that the teratogenic antibodies localized within the large phagolysosomes and the apical vesicles of the visceral yolk-sac endoderm. It is postulated that visceral yolk-sac pathology was induced by the antibodies.

Animals↗
PubMed1984

Effect of short-term exposure to five industrial metals on the embryonic and fetal development of the mouse.

An increase is expected in the world's industrial use of several metals, Al, Co, Mo, V, and W, among others. Very little is known about their possible effects on early mammalian development. Groups of mice were injected with compounds of these metals either before implantation or at early organogenesis. None of the metal compounds showed any interference with implantation, but all of them significantly affected fetal development: Al caused an increased frequency of fetal internal hemorrhage, Mo inhibited fetal normal weight gain, W increased the frequency of resorptions, and Al, Co, Mo, and V all interfered with fetal skeletal ossification.

Animals↗
PubMed1982

Isolation, partial characterization, and localization of a rat renal tubular glycoprotein antigen. Antibody-induced birth defects.

A glycoprotein with an apparent 340,000 mol wt (gp 340K) was isolated from rat kidney saline-soluble extract by ammonium sulfate precipitation, DE 52 ion-exchange cellulose chromatography, concanavalin A affinity column, Sephacryl S-300 gel filtration, and discontinuous polyacrylamide gel electrophoresis (PAGE). The relative purity of gp 340K was examined by double immunodiffusion analysis, disc PAGE, and immunoelectrophoresis. Injection of rabbit gp 340K antiserum into pregnant rats during the organogenetic period induced abnormal embryonic development, fetal growth retardation, and embryonic death. Antiserum against the immunocomplexes isolated by immobilized protein A also produced the same embryotoxic effects. The biologic effects of the antisera appeared to be dose dependent. Defects such as anophthalmia, hydrocephaly, exencephaly, cleft palate, cleft lip, and some cardiovascular anomalies were observed. The most frequently observed anomaly was anophthalmia. Immunofluorescent localization studies indicated that gp 340K antibodies localized in vivo in the visceral yolk-sac endodermal cells and the embryonic endoderm. In vitro immunofluorescent localization studies revealed that gp 340K was a component of the renal tubular cells that cross-reacted with antigen in the visceral yolk-sac endodermal cells and embryonic endoderm. The underlying mechanism whereby gp 340K antibodies induce birth defects is not known. Three hypotheses were discussed.

Animals↗