ABSTRACT
We have obtained hybrids of PCC4-aza 1, a mouse embryonal carcinoma stem cell line, and two different thymidine kinase deficient mouse cell lines. We have examined the ability of the parental and hybrid cells to produce interferon after infection with the Newcastle Disease virus and to enter the antiviral state when treated with mouse interferon. The interferon system of PCC4-aza 1 is inactive; this characteristic is recessive in the hybrids obtained.
Subject(s)
Hybrid Cells/metabolism , Interferons/biosynthesis , Teratoma/metabolism , Cell Differentiation , Cell Line , Chromosome Mapping , Genes, Recessive , Interferons/genetics , KaryotypingABSTRACT
The expression of the interferon-induced antiviral state was studied in heterokaryons and cytoplasmic hybrids (cybrids). An autoradiographic assay for the antiviral state, in which the percentage of cells containing vaccinia viral DNA factories was determined, was used. The expression of the antiviral state was dominant in homokaryons and heterokaryons formed by fusion of interferon-treated cells with untreated cells. Cytoplasts derived from treated cells conferred resistance to virus growth on cybrids formed by fusing such cytoplasts with untreated cells. Treatment of L cell x HeLa cell heterokaryons with human interferon or mouse interferon was much less effective in inducing a detectable antiviral state than was similar treatment of parental cells with homospecific interferon. The antiviral state was fully induced when heterokaryons were treated simultaneously with both types of interferon. Cybrids formed by fusing L cell cytoplasts with HeLa cells or HeLa cytoplasts with L cells did not enter a detectable antiviral state after treatment with interferon specific for the cell type of the enucleated parent. However, treatment of cybrids with interferon specific for the cell type of the nucleated parent was effective in inducing a detectable antiviral state.
Subject(s)
Hybrid Cells/drug effects , Interferons/pharmacology , Vaccinia virus/growth & development , Animals , HeLa Cells/drug effects , Humans , L Cells/drug effects , Mice , Species Specificity , Virus ReplicationABSTRACT
Pregnancy is terminated in rats that have mated at the postpartum oestrus if they are allowed to suckle a large litter after implantation. For consistent termination, the number of sucking young must be at least nine, the accelerated lactation must be begun before Day 10 of pregnancy, and must be continued for at least 2 days.
Subject(s)
Embryo Loss/etiology , Fetal Death/etiology , Lactation , Litter Size , Rats/physiology , Animals , Embryo Implantation , Embryonic Development , Estrus , Female , Male , Pregnancy , Uterus/anatomy & histologyABSTRACT
The activity of 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD) was assayed in the ovaries of rats after accelerated lactation to determine its relationship to the decrease in progesteron secretion that occurs. When rats were sjbjected to accelerated lactation on Day 9 of pregnancy, activity of the enzyme was only slightly increased by Day 10, but had risen to twice the control level by Day 11, and three times the control level by Day 12. Administration of LH or progesterone prevented the increase in enzyme activity. Progesterone concentration had decreased considerably before the time at which any significant increase in 20alpha-HSD activity was detected. These findings are discussed in relation to the role of 20alpha-HSF in regulating progesterone levels in the rat.
Subject(s)
Embryo Loss/enzymology , Fetal Death/enzymology , Hydroxysteroid Dehydrogenases/biosynthesis , Lactation , Ovary/enzymology , Progesterone/blood , Rats/physiology , Animals , Embryonic Development , Female , Luteinizing Hormone/pharmacology , Pregnancy , Progesterone/pharmacology , RadioimmunoassayABSTRACT
The relationship was investigated of the hormones associated with pregnancy and lactation and the termination of pregnancy that occurs when rats mated at the post-partum oestrus are allowed to suckle a large litter after implantation. The primary cause for pregnancy termination was found to be an insufficient level of progesterone with the possible need for a primary or synergistic dose of oestrogen. The progesterone deficiency was not due to the high levels of prolactin present in nursing rats, since pregnancy termination could not be produced by prolactin administration in the absence of accelerated lactation, and could not be prevented by blocking prolactin secretion after accelerated lactation. Administration of LH to rats after accelerated lactation did prevent termination of pregnancy.
