Embryonic mortality caused by maternal heat stress during mouse oocyte maturation

Abstract

The effects of maternal hyperthermia during meiotic maturation were studied in oocytes and foetal mice. Heat stress was induced by exposure to 35 ± 1°C and 65 ± 3% RH for 12.5 h. Embryos of uniform chronological age were produced by pairing with non-stressed males for a limited mating period. The morphology and cytogenetic constitution of oocytes were analysed and correlated. Meiotic maturation was disrupted in 39.8% of analysable ova of heat-stressed females. Heat-stressed ova stopped maturing at diakinesis-metaphase I in 4% and polar body chromosomes were retained in 2% of treated ova. Oocytes with atypical morphology were almost always ( r=0.96) cytogenetically aberrant. At 19 days of gestation, pre-implantation losses were increased (16.2% for heat-stressed vs. 4.9% for control), but the greatest increase in embryo mortality occurred soon after implantation (34.4% for heat-stressed vs. 11.7% for control), indicating induction of dominant lethal mutations. Individual response to stress was highly variable, ranging from total pre-implantation loss (10 animals) to control levels. Heat-stressed dams with implantations produced only 67% as many foetuses as the control dams. This suggests that genetic aberrations are induced in maturing oocytes by maternal heat stress of short duration and that these alterations do not cause immediate loss of ova or embryos. Instead, a large proportion of the ova produced embryos capable of implantation but not capable of continued development. These large embryo losses result in increased numbers of pregnancies that would be uneconomical to maintain in agricultural species.