No abstract

An ultrastructural investigation was made of cell death in the uterine epithelium during the implantation of the mouse blastocyst. Cell death occurs in two phases: (i) early individual cell death, and (ii) later general cell death. Individual dead epithelial cells are phagocytosed and digested by trophoblast cells. At 95 h post coitum (p.c.) there are 1–4 dead cells; at 105 h and 113 h, 6–8 dead cells, and at 116 h, 2–3 dead cells. No lysosomal involvement could be identified in the death of these cells. The general breakdown of the uterine epithelium around the implanting blastocyst is first recognizable at the ultrastructural level at 113 h p.c, and continues until the adjacent deteriorated epithelium has been phagocytosed by the trophoblast cells at 119 h p.c. Ultrastructurally, from 113 h p.c. cytoplasmic portions of epithelial cells are trapped within cytosegrosomes, and there is an increase in size of the dense lysosomal bodies found in viable epithelial cells at 105 h p.c. The dense bodies, which are positively stained for acid phosphatase enzyme at 105 h p.c, increase in diameter approximately 3–5 times between 105 h p.c. and 119 h p.c. These results provide evidence of intracellular digestion of small portions of the cytoplasm possibly through the formation of cytosegrosomes which then fuse with residual bodies already present. Thus the evidence favours a process of autolytic breakdown of the uterine epithelium around the implanting blastocyst.

The present study investigates the effects of different doses of "trichloroethylene" TCE on pregnancy, early embryos on days 6 and 8 of pregnancy. The experimental females (90 virgin females) were divided into three groups; the first one (C) was the control that treated with the solvent only (corn oil), the second (G1) and the third (G2) treated groups with low (24 mg/kg) and high (240 mg/kg) dose of TCE, respectively. Oral administration of TCE to female mice once daily for a period of 21 days before mating and till 5 th and 7 th day of pregnancy, caused a significant decrease in the body weight for non-pregnant females and weight gain for pregnant females. The percentage of survival, mating and abortion were also significantly decreased by TCE treatment for pregnant females. Histological examination for the obtained 6 and 8 day mice embryos from treated mothers showed some histopathological alterations in compared with the normal control embryos. These alterations indicated that TCE treatment resulted in retarded, delayed and deformed embryos. The results suggest that TCE has teratogenic and embryo toxic effects on the early development of mice embryos following a short-term of exposure.

In the zona pellucida-intact 95 h post coitum mouse blastocyst, electron-microscopic studies reveal the presence, as a part of normal development, of 1–2 dead cells lying free on the surface of the inner cell mass (ICM) or trophoblast cells, and of 4–5 dead cells phagocytosed by 1CM cells. Such dead cells are electron-dense and show characteristic chromatopycnosis of the nucleus, and swelling of the endoplasmic reticulum. In addition, 1–2 digestive vacuoles with granular contents and myelin figures are found, principally in ICM cells, and corresponding with basophilic bodies observed with the light microscope. The results are interpreted as indicating that a relatively large number (i.e. a minimum of 6–8, or approximately 10%) of blastocyst cells die and are phagocytosed and digested, usually by the ICM cells, but probably also by trophoblast cells. This process does not, however, affect the future differentiation of the ingesting cell. Simultaneously a small number of epithelial cells adjacent to the blastocyst die, either singly or in small groups. These findings confirm the view that previous reports of penetration of the uterine epithelium by ‘primary invasive cells’ originating in the ICM were due to confusion between two separate groups of dead cells, namely the embryonic dead cells of the ICM and the single dead cells in the adjacent uterine epithelium, which appear to be phagocytosed by trophoblast cells following loss of the zona pellucida.