Disease relevance of Embryo Loss

• This pattern can be interpreted as resulting from two bacterial effects: One (usually termed mod, for modification) would affect sperm and induce embryo death, unless Wolbachia is also present in the egg, which implies the existence of a second effect, usually termed resc, for rescue [1].
• High rates of egg infertility and embryo death in a colony of South Polar Skuas breeding in the Antarctic were similar to those in polluted North Atlantic populations of the Great Skua [2].

High impact information on Embryo Loss

• Pregnant CBA/J females mated with DBA/2 males (20-30% early embryo loss) and CD1 females mated with CD1 males (5-10% early embryo loss) were studied on days 8, 10, and 12 of gestation [3].
• Preconceptional paternal exposure to cyclophosphamide, a widely used anticancer agent, leads to increases in embryo loss, malformations, and behavioral deficits in offspring; these abnormalities are transmissible to subsequent generations [Auroux, M., Dulioust, E., Selva, J. & Rince, P. (1990) Mutat. Res. 229, 189-200] [4].
• Targeted disruption of mouse centromere protein C gene leads to mitotic disarray and early embryo death [5].
• These results showed, for the first time, a correlation between increased iNOS and TNF-alpha expression and embryo resorption [6].
• Protamine 2 deficiency leads to sperm DNA damage and embryo death in mice [7].

Chemical compound and disease context of Embryo Loss

• Embryo loss was associated (p = 0.01) with increased serum concentrations of progesterone in recipients at the time of transfer [8].
• Phosphoramide mustard alone, at concentrations of 10 and 25 microM, did not produce embryo deaths but did cause malformations and growth retardation in 100% of the exposed embryos [9].
• Day 10 rat embryos were cultured in the presence of acrolein and glutathione, either concurrently or sequentially, and evaluated for embryo deaths, malformations, growth retardation, and content of glutathione and protein [10].
• The addition of 10 microM buthionine sulfoximine resulted in 100% embryolethality at 100 microM acrolein; this buthionine sulfoximine concentration decreased the EC50 values for embryo deaths and malformations to 50% of those for acrolein alone [9].
• 4-Hydroperoxycyclophosphamide produced embryo deaths and malformations and decreases in embryonic growth and protein content at concentrations in the range of 5 to 25 microM [11].

Biological context of Embryo Loss

• In contrast, embryo resorption was boosted after ASGM1 injection, and correlated subsequently with a smaller litter size [12].
• On the day of insemination, peripheral estrogen was significantly higher (P < 0.05) in the early embryo loss group (15.3 +/- 1.1 pg/mL, n = 27) than in pregnant (9.4 +/- 0.6 pg/mL, n = 26) or not pregnant (9.6 +/- 0.7 pg/mL, n = 25) group [13].
• Overall, the results indicate that suboptimal progesterone support during the early luteal phase is likely to deleteriously affect embryo viability and in addition, that it is possible to predict milk progesterone concentrations during the early luteal phase based on earlier stage concentrations and thus identify cows at risk of early embryo loss [14].
• In addition, embryo death in SCP3-deficient females increases with advancing maternal age [15].
• Female germ cell aneuploidy and embryo death in mice lacking the meiosis-specific protein SCP3 [15].

Anatomical context of Embryo Loss

• This suggested that IFN-gamma was needed for LPS-induced embryo resorption and that decidual macrophages from pregnant GKO mice were not primed and could not be activated when given LPS [16].
• Injection into fertile chicken eggs of synovial fluids from some rheumatoid arthritis patients resulted in either embryo death or the development of the "crooked-toe" (CT) syndrome, or both, in newly hatched chicks [17].
• In the course of experiments on the effects of anabolic steroids on the myocardium of rat conceptuses, we found that subcutaneous implantation of 10 mg of estradiol, Dianabol or testosterone to rats in mid pregnancy, resulted in embryo resorption [18].
• The objective of this study is to investigate the significance of natural killer (NK) cells and interleukin-2 in uterus in the early embryo loss (or resorption), and to elucidate the immunological modulation of maternal-fetal interface with Chinese herbal medicine Radix scutellariae (huang qin) and Rhizoma atractylodis (bai zhu) [19].

Gene context of Embryo Loss

• This is to our knowledge the first study correlating the increase in post-implantation embryo loss obtained after paternal drug treatment with the decrease in the expression of Igf2 in these embryos [20].
• This suggests that SAPKgamma/JNK1 and SAPKalpha/JNK2 may be important mediators of stress-induced responses in early implanting conceptuses that could mediate embryo loss [21].
• On the other hand, far fewer of the CBA/J x Balb/c conceptuses (5-10% embryo loss) displayed significant cellular infiltration and nitric oxide and TNF alpha [22].
• INTERVENTION(S): The administration of polyIC was performed to establish a murine model of induced embryo resorption, with or without TLR3 blocking by multiple injection of mAb against this receptor [23].
• The results obtained confirmed the embryotoxic character of NO found in these particular sera leading to the hypothesis that NO plays a potential role in early embryo death [24].

References