Incorporation of [3H] Uridine by Mouse Embryos with Abnormalities Induced by Parental Hyperthermia

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Abstract
Albino ICR mice were used in a factorial experiment to study the incorporation of [3H]uridine by embryos exhibiting abnormal development induced by a 24 h exposure of parent mice to an ambient temperature of 34.5.degree. C and 65% relative humidity. Embryos recovered from females killed at 64, 72, 88 and 96 h after HCG [human chorionic gonadotropin] were pulse-labeled by incubating in culture medium containing [3H]uridine for either 5 h (2 cell), 90 min (4 cell), 45 min (8 cell), 20 min (morula) or 10 min (blastocyst). The incorporation of [3H]uridine was examined by autoradiography. Following exposure of the parental female to high temperature approximately 40% of the embryos are arrested at the 2-cell stage and fail to incorporate [3H]uridine. An additional 20% of the 2-cell embryos are only partially affected in that 1 blastomere is able to undergo a limited number of cleavage divisions. The cleaving blastomeres of these embryos demonstrate a distribution of isotope comparable to the blastomeres of normal embryos at the same chronological stages of development. In contrast, the incorporation of isotope into the arrested blastomere, if it occurs, is confined to the nucleus and never assumes the pattern typical of blastomeres at later stages of development. Paternal hyperthermia, an effect conveyed by the fertilizing spermatozoan, allows normal embryonic development during the early cleavage stages. The rate of development is retarded at the morula stage although blastulation eventually occurs. A significant proportion of embryos at the 8-cell and morula stages also contain blastomeres which fail to incorporate the isotopic precursor. Consequently, the retardation in embryonic development is preceded by a partial failure to synthesize RNA. These embryos may be responsible for the embryonic mortality known to occur at, or shortly after, implantation.