Adult female mice of the "sensitive" NMRI/Han strain ovulate diploid oocytes after gonadotropin treatment. Other mouse strains are "non-sensitive" with respect to the ovulation of such diploid oocytes. In this study we combined the impaired ovarian situation in the XO karyotype with the trait "diploidy", which is determined genetically, by mating Ta/O (Ta = Tabby) females of C3H X 101 background to males of the NMRI/Han strain. The adult female F1 hybrids were stimulated to ovulation by gonadotropins and identified by their karyotype (XX or XO). The cytogenetic analysis of ovulated oocytes revealed a low level of diploidy in the XX littermates (1.0%), but a very high level in females with the XO karyotype (24.6%). All of the XO females ovulated at least one diploid oocyte. We suggest that it is the XO status which drastically impairs meiosis I in our "gonadotropin-sensitive" F1 females due to (1) alterations of the developmental program within the oocyte, (2) a disturbed communication between oocyte and follicle, (3) a preferential maturation and ovulation of "follicles at risk", or (4) an exceptional recruitment of many such follicles, by, e.g., a premature responsiveness to gonadotropins in our XO females. An interdependence of several such mechanisms is possible.