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PubMed1981

Effect of high molecular levan on implantation and embryonic development in mice.

Pregnant Balb C mice were treated daily with levan beginning on either the first or the ninth day of pregnancy. Damage to embryos appeared on the eighth day in mice treated from the first day. In the second group, the damage was apparent two to four days after the levan treatment was begun. In both groups the damaged and dead embryos were found side by side with apparently normal conceptuses. The damage seems to have been caused by lesions to the trophoblast since it only occurred after implantation and placentation, and it appeared to be different from the antitumoral or the graft-rejection delaying effects of levan.

Animals↗
PubMed1995

[The toxic effect of serotonin in direct and mediated actions on rat embryos].

Embryotoxic effect of serotonin in direct (intra-amniotic administration) and indirect (subcutaneous administration) treatment was studied. In both cases serotonin causes embryo death and different abnormalities in development in small number of embryos. Mechanism of serotonin embryotoxic effect is under discussion.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

[The embryotoxic effect in rats exposed to the blood serum of newborn infants tested for the presence of transfer factors].

Pregnant rats (day 14 of gestation) received intraamniotic injections of newborn human serum. Transfer factors (TF) present in injected serum produced significant embryotoxic and teratogenic effects, as well as changes in coordination of motor activity (EMG) in newborn rats. The extent of embryological disturbances and the motor activity of 33- to 34-day old recipient rats depend on TF concentration (at serum dilution 1:2) and on the state of infant's motor functions ("normal" group and "risk" group). The results obtained allow to objectively determine the pathogenic effect of serum TF on embryotoxicity and formation of motor coordination in the donor infant.

Abnormalities, Drug-Induced↗
PubMed1996

Toxicity to transferred rat embryos after aspirin treatment during preimplantation stage in vivo.

AIM: To explore the relationship between drug-induced blastopathies and post-implantation embryotoxicity or developmental defects. METHODS: Pregnant rats on d 3 were given intragastrically aspirin (0.25, 0.5, and 1 g.kg-1). On d 4, the blastocysts were transferred into the uterine horns of pseudopregnant rats (made by mating with male rats which had been given intragastrically 3-chloro-1,2-propanediol 5 mg.kg-1 for 5 d). Uterine contents were examined at term. RESULTS: The frequency of blastocysts with morphological alterations (FBMA) was increased on d 4 of gestation. The implantation rate was lower than that of the controls. A dose-related increase in resorption (55.2%, 69.5%, and 85.2%) and malformation rate (3.8%, 44.4%, and 25%), and decrease in viability rate of fetuses (44.8%, 30.5%, and 14.8%) were observed in test groups with correlations to FBMA. CONCLUSION: Embryotoxicity and fetal malformations were induced by treatment of aspirin before implantation in a dose-dependent manner.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

[Embryo survival rate of BALB and C57BL line mice in reciprocal transplantations at early stages of development].

Survival rate and weight were studied for the BALB/c and C57Bl/6J mice embryos developed from transplanted 2- and 3-day-old blastocysts. The greatest number of implantations was observed when 3-day-old blastocysts were transplanted to recipient females with two-day pregnancy. The number of implantations and successfully developing transplanted embryos was increased in recipient female with a higher number of corpora lutea.

Animals↗
PubMedDate not supplied

[Ultrafast freezing of the embryos of outbred and inbred mouse strains].

Survival of 8-cell mouse embryos of inbred strains C57B1 and DBA and outbred strain NMRI was studied after ultrafast freezing. The embryos were placed in 10% glycerol for 10 min, transferred in plastic tubes filled with a mixture of glycerol and 1 M sucrose (3:7), and immersed in liquid nitrogen within 1.5 min. The tubes were thawed in air at the room temperature, the embryos were washed in 0.5 M sucrose and cultivated in a Dulbecco medium with 20% fetal calf serum at 37 degrees C for 48 h or transplanted to recipient females. The survival of embryos was estimated according to their capacity to develop in vitro to the blastocyst stage or form normal fetuses after transplantation. After thawing and cultivation, 80.4% of NMRI embryos retained viability (80.7% in the control). For C57B1 and DBA embryos, these indices were 90.2 and 88.7%, and 59.3 and 66.7%, respectively. The differences between the experiment and control was insignificant for all strains. After thawing and transplantation of NMRI embryos, 34.4% developed into normal live fetuses (in the control 33.3%). At the same time, after cryoconservation by the standard method using a programmed freezer, the viability of ICR and NMRI embryos decreased approximately by 20% even in in vitro experiments. Thus, no differences were found in survival of the embryos of the studied strains after ultrafast freezing. This method proved to be very efficient for the embryos of both inbred and outbred mouse strains, since their capacity for development practically did not decrease after cryoconservation. The method may be used for production of cryobanks of embryos of various mouse strains.

Animals↗
PubMed1997

A study of early pregnancy factor activity in preimplantation.

PROBLEM AND METHOD: Early pregnancy factor (EPF), an Immunosuppressive substance, which appears in pregnant women's sera 48 h after fertilization, is a kind of pregnancy-specific protein. To determine whether the EPF activity could be a super early indicator of pregnancy, we used rosette inhibition assay to detect EPF activity in the sera, collected from 70 women 2-7 days after ovulation intending to conceive monitored by ultrasonography. Simultaneously we selected 40 non-pregnant sera and 12 early-pregnant sera as negative control and positive control, respectively. RESULTS: The results of this study demonstrated that EPF activity is detected in 35 women's sera out of 70 women within 2-7 days after ovulation, and 28 women out of the 35 were pregnant, which was known by follow-up, and 7 were not pregnant, possibly due to either false positive results or embryo loss because of preimplantation failure, thus causing no pregnancy. The other 35 out of 70 had no EPF activity and 34 of them were not pregnant, which was known by follow-up, but one case became pregnant, which was false negative result. Our study showed that diagnosis of the super early pregnancy could be made by detecting EPF activity in maternal serum within the time of preimplantation. The accuracy of pregnancy diagnosis by this method is 88.6%, with a false negative rate of 3.4% and a false positive rate of 17.1%. The beta-HCG level was measured from the above 70 women's sera in order to contrast EPF activity. All of the sera collected 2-6 days following ovulation indicated that there were lower beta-HCG values in very early pregnancy (> or = a5 mIU/ml). On the seventh day after ovulation, EPF activity was detected in 11 out of 15 sera with only 2 of them with a b-HCG level that reached or slightly surpassed that of the early pregnancy diagnosis (5 mIU/ml and 5.4 mIU/ml, respectively). This demonstrated that beta-HCG is not the earliest signal of pregnancy; otherwise the EPF activity is one that appears 2-6 days earlier than beta-HCG appears. We measured the progesterone level of the 48 sera from the 70 collected above within 2-7 days postovulation and found most of them reached the level of progesterone in the luteal phase (7.5-98.3 nmol/L). This indicated that ovulation had taken place in these women, which was in accordance with observations by ultrasonography. CONCLUSIONS: Our study showed that diagnosis (of 88.6%) of super early pregnancy could be made with an accuracy of 88.6% by detecting EPF activity in maternal serum within 2-days after ovulation. This offers a basis for pregnancy diagnosis for the women who attempt to terminate their pregnancy safely or who conceive unexpectedly, and it contributes to family-planning.

Adult↗
PubMed1996

[Effects of blastocyst deficiencies induced by aspirin treatment during preimplantation period in rats on development of embryos after implantation].

Pregnant rats were treated orally with aspirin 0.5 or 1.0 g.kg-1 on d 3 (positive vaginal smear was considered as d 0) and were sacrificed on d 4. Some blastocysts collected on d 4 were evaluated for gross morphology and cell number, and the remainings were transfered into pseudopregnant rats. Results showed that the rate of blastocysts with abnormal morphology were 23.8% and 40.8%, respectively, in 0.5 and 1.0 g.kg-1 of aspirin. These were significantly higher than 6.8% of the control group. The cell number of blastocysts also decreased in the aspirin groups. The rate of implantation and live fetuses in the case of blastocysts with normal morphology were related negatively with the aspirin doses, espesially in the group of 1.0 g.kg-1 of aspirin, the implantation rate was significantly lower (38.6%). However, the implantation rate of blastocysts with abnormal morphology in both groups of aspirin were much less than that of the control group, and all embryos after implantation were resorped. No significant malformations were observed in the live fetuses. These results suggests that the effects of blastocyst deficiencies induced by aspirin on development of embryos transfered into pseudopregnant rats mainly caused death of embryos, but not malformation of fetuses.

Animals↗
PubMed1977

The effect of Imuran on implantation and early embryonic development in rats.

Pregnant rats were injected daily with 2, 4, and 20 mg/kg of Imuran from the first day of gestation until sacrificed on Days 6-12. Gravid uteri, as well as maternal organs, were removed and examined histologically. According to the histologic findings, the treatment with the high dose of 20 mg/kg/day Imuran induced injuries to the blastocyst. Starting from Day 8, the trophoblastic layer lost its continuity and maternal blood invaded into the blastocystic cavity resulting in destruction of embryonic tissues. This degeneration progressed until evident resorption on Day 12. Smaller doses, such as 2 or 4 mg/kg of Imuran, did not result in early trophoblastic damage. The effect seemed to be the result of the antimetabolic effect of Imuran acting on the proliferating trophoblast through the maternal blood.

Animals↗
PubMed1997

Heteropagus conjoined twins due to fusion of two embryos: report and review.

We report on a case of conjoined twinning (CT) consistent with fusion of two embryos followed by resorption of the cranial half of one of them, resulting in a normal male baby with the lower half of a male parasitic twin fused to his chest. Fluorescent in situ hybridization (FISH) studies suggested that the parasitic twin was male, and DNA typing studies demonstrated dizygosity. Although incomplete fission is the usual explanation for conjoined twins, the unusual perpendicular orientation of the parasite to the autosite supports a mechanism observed in mares in which early fusion of two embryos is followed by resorption due to compromised embryonic polarity.

Abnormalities, Multiple↗
PubMedDate not supplied

Variability of embryonic development among three inbred strains of mice.

We examined the relationships between litter size, embryonic growth, days of gestation, onset and duration of morphological stages and development of the first arch skeleton in three inbred strains of mice--C57BL/6, CBA/J and C3H/He. Detailed embryonic staging was based on craniofacial development between 11 and 18 days of gestation. Considerable intra- and interlitter variation of morphological stages of embryonic development exists in all three inbred strains. The relationship of morphological stages to days of gestation reveals that each stage has a different duration, being shortest at Theiler's stage 18 and longest at stage 21 in all three inbred strains. Embryos of CBA/J mice tend to reach each stage later than do embryos of the other two strains, i.e., morphological development is slowest in CBA/J. The greatest length, a measurement of embryonic growth, increases at a constant rate during gestation in all three strains. In C57BL/6 and CBA/J, more embryos tend to be implanted in the right horn of the uterus than in the left, whereas in C3H/He an even number of embryos tends to be implanted in both horns. Timing of the development of Meckel's cartilage differs between the three inbred strains: both condensation and onset of matrix deposition begin one stage earlier in C57BL/6 than in CBA/J and C3H/He. On the other hand, alkaline phosphatase, one of the earliest markers for bone development, is expressed at the same time in all three inbred strains. Differences in timing of skeletal development between the strains may be attributed in part to the genealogical closeness OF CBA/J and C3H/He mice.

Animals↗
PubMed1998

Developmental neurotoxicity and immunotoxicity of 2,4,6-tribromophenol in Wistar rats.

Pregnant Wistar rats were exposed to 2,4,6-Tribromophenol (TBP) by whole body inhalation (0, 0.03, 0.1, 0.3, 1.0 mg/m3, 24 hr/day, 7 days/weeks, from day 1 to 21 of gestation). Significant decreases in orientation reactions were noted at concentrations of 1.0 mg/m3 (p < 0.05) in the open field test. Nonsignificant trends (p > 0.05) toward decreased horizontal movement and emotionality in the open field and increased electrical impulse skin pain threshold (SPT) were observed. No significant exposure-related differences in the nonspecific immunological status (phagocytosis and blood anti-microbe activity) of pregnant rats were seen after the exposure. Preimplantation and postimplantation embryo losses were significantly increased in a dose-dependent manner and were seen in all treated groups except the lowest concentration (0.03 mg/m3) group. Signs of retarded fetal skeletal development and increased frequencies of visceral abnormalities were found at concentrations of 0.1 and 1.0 mg/m3. Significant effects were found for lower incisor eruption and ear unfolding at a concentration of 0.3 mg/m3. The grooming behavior of 30-day old male progeny was significantly less than control in all experimental groups. Grooming behavior in female subjects exposed to a concentration of 0.3 mg/m3 and emotionality in subjects exposed to a concentration of 1 mg/m3 were decreased significantly. At 60 days of age emotional reactions were significantly decreased in female subjects from the 0.03, 0.3 and 1.0 mg/m3 groups. SPT was significantly increased in the 1 mg/m3 group for both male and female pups. Thus, evidence of CNS depression influence of TBP both in maternal and offspring groups was found. The NOEL (No Observed Effect Level) for developmental neurotoxicity is thus < 0.03 mg/m3, and the NOEL for maternal neurotoxicity is 0.3 mg/m3. These results suggest that exposure to TBP for 24 hr/day throughout gestation may cause developmental neurotoxicity, embryotoxicity and fetotoxicity, but not immunotoxicity.

Animals↗
PubMed1976

[Studies on the prenatally toxic effect of parathionemethyl in Wistar rats compared to cyclophosphamide and trypan blue].

Higher yield and performance in plant and animal production will depend on reinforced use of pesticides, particularly alkyl phosphate esters and insecticidal carbamates. Prenatal toxic action of the pesticides used today may be detrimental to human and animal health. Prenatal-toxicological tests, using parathion-methyl, were conducted on the basis of known but modified experimental methods. The vulnerability of a rat strain was tested by applying to it teratogenic model substances (trypan blue and cyclophosphamide). Several oral applications of parathion-methyl (3 ppm) during the sensitive phases of germ formation and growth (fifth to ninth and eleventh to fifteenth or eleventh to nineteenth days from conception) were followed by clear embryotoxic effects, such as retardation and increased resorption. The average number of resorption sites grew from nine in the control group to 20 in the experimental group. Postnatal malformations were not observed.

Abnormalities, Drug-Induced↗
PubMed1976

Placental agenesis, embryonal hydraemia, embryolethality and acute hypervitaminosis A in rats.

Acute maternal hypervitaminosis A established on Day 9 of gestation in Sprague-Dawley-derived rats caused a dose-related increase in the resorption of implants. The median embryolethal dose was 189,000 i.u./kg. In addition to suppression of the allantois leading to placental agenesis, damaged embryos showed retarded somatic development and hydraemia, all apparent 24 h after treatment. At about Day 11 the hydraemia involved the visceral wall of the yolk sac causing death of the embryo soon after. The fluid in the vitelline vessels continued to collect until Day 13 when it absorbed following necrosis of the wall of the yolk sac. Two mechanisms are suggested for the embryonal hydraemia: either the excess fluid resulted from a permeability disorder induced by the vitamin A; or it was retained metabolic water or water specifically absorbed to inflate the allantois and, being unused for this purpose, it pooled in the blood vessels of the embryo. The yolk sac hydraemia is more likely to have followed injury to the proximal endoderm.

Abnormalities, Drug-Induced↗
PubMed1999

Sex ratio bias in postpartum-conceived Norway rat litters is produced by embryonic loss in midpregnancy.

In rats, dams that conceive in their postpartum oestrus and then lose their firstborn litter bias the sex ratio of the litter toward females in utero. The present study identifies the source of litter sex ratio bias in these postpartum pregnant non-lactating dams. The female bias arises first through the postconception loss of embryos, and second, the loss occurs in midpregnancy between the attachment of the blastocyst to the uterine wall on day 5 and full metrial gland development on day 14. Some pregnancies were restricted to one uterine horn to see if this loss (and thus the opportunity for litter sex ratio biasing) was influenced by local factors operating within the uterine horn. Embryonic loss was more closely associated with the number of embryos implanting in a single horn than with the number implanting in the litter, demonstrating that local crowding within a horn is sufficient for the preferential loss of male embryos. This loss did not cause an obvious decrease in the size of the live-born litter because only those horns with a surfeit of embryos lost them. This process was the same in the right and left horns; both carried and lost the same numbers of embryos. A dam that conceives in her postpartum oestrus and then loses her suckling litter forgoes the implantation delay and uterine healing caused by lactation. Male embryos are less successful at implanting in a uterus only recently vacated by a previous litter.

Animals↗
PubMed2002

Rescue of neural tube defects in Pax-3-deficient embryos by p53 loss of function: implications for Pax-3- dependent development and tumorigenesis.

Pax-3 is a transcription factor that is expressed in the neural tube, neural crest, and dermomyotome. We previously showed that apoptosis is associated with neural tube defects (NTDs) in Pax-3-deficient Splotch (Sp/Sp) embryos. Here we show that p53 deficiency, caused by germ-line mutation or by pifithrin-alpha, an inhibitor of p53-dependent apoptosis, rescues not only apoptosis, but also NTDs, in Sp/Sp embryos. Pax-3 deficiency had no effect on p53 mRNA, but increased p53 protein levels. These results suggest that Pax-3 regulates neural tube closure by inhibiting p53-dependent apoptosis, rather than by inducing neural tube-specific gene expression.

Animals↗
PubMed1995

Anordiol and RU486 synergize to produce preimplantation pregnancy loss by increasing embryo transport (rat).

RU486, an antiprogestational agent, and anordiol (dihydroxylated metabolite of anordrin) which has an estrogenic and antiestrogenic activity, are known to inhibit fertility. These agents were administered orally, alone or together, to rats prior to implantation, on Day 2 of pregnancy. Control animals were fed with the vehicle only. The effectiveness of the agents in terminating pregnancy in female rats was determined on Day 14 of pregnancy. Anordiol presented a dose-dependent effect on abolishing pregnancy, being 100% effective at 2.5 mg/Kg and non-effective at 0.6 mg/Kg. RU486 did not prevent pregnancy even at a dose of 4 mg/Kg. Doses of RU486 and anordiol that were ineffective when administered alone, prevented pregnancy in 70% of the rats when these agents were given together. To determine the mechanism by which these drugs prevent pregnancy, oviducts and uteri of rats were examined for presence of embryos on Day 3 of pregnancy. Only 29% of embryos were recovered from the oviducts of rats treated with 2.5 mg/Kg anordiol (compared to 89% in control group) plus an additional 9% from the uteri. In combination, anordiol and RU486 had a synergistic effect on embryo transport in the rats' reproductive tract, without any apparent accumulation in the uterus. These results led us to conclude that the pregnancy preventing action of anordiol plus RU486 is mostly due to accelerated transport of the embryos in the reproductive tract prior to implantation.

Abortion, Induced↗