Fertilization and early embryonic development subsequent to mating with TEPA-treated male mice.

FTER parental exposure to mutagens and subsequent mating, adverse A genetic effects may manifest sequentially by preimplantation losses of fertilized ova and zygotes, early fetal deaths, and sterility and semisterility in F, progeny ( CATTANACH 1964; EPSTEIN et al. 1970a). Effects of ionizing irradiation of the male or of sperm in uitro on fertilization and subsequent development of the zygote have been extensively studied in the rabbit (AMOROSO and PARKES 1947; CHANG, HUNT and ROMANOFF 1957; BEDFORD and HUNTER 1968), and in the mouse (BRENNEKE 1937; BRUCE and AUSTIN 1956; EDWARDS 1957); such data are comparatively rare for chemical mutagens, although antifertility effects of alkylating agents, manifested by reduced litter sizes, are well recognized (JACKSON, Fox and CRAIG 1961; JACKSON 1966). Embryos with chromosomal damage have been demonstrated following artificial insemination of mice with spermatozoa treated with nitrogen mustard in uitro (EDWARDS 1958). Following treatment of male mice with triethylenemelamine, antifertility effects were shown to be due to induction of dominant lethal mutations resulting in early fetal deaths, and to reduced fertilization in postmeiotic and premeiotic matings, respectively (CATTANACH and EDWARDS 1958). Administration of chemical mutagens to female mice prior to ovulation produced genetic damage, histologically recognizable as early as the 2-cell zygote stage ( GENEROSO 1969). Dose-dependent mutagenic effects have been demonstrated following treatment of male mice with triethylenephosphoramide and other alkylating agents (EPSTEIN and SHAFNER 1968; EPSTEIN et al. 1970a, b) . We report here data on fertilization and early embryonic development in mice following paternal treatment with a single dose of TEPA, and subsequent mating over the duration of the spermatogenic cycle.