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Androgen-dependent urinary constituents from males hasten reproductive maturation (the Vandenbergh effect) and disrupt peri-implantation pregnancy (the Bruce effect) in nearby females. Each of these effects can be mimicked in socially isolated females by direct administration of exogenous oestrogens. The current experiments were designed to determine the role of males' urinary 17β-oestradiol (E(2)) in their capacities to induce these effects. A preliminary experiment showed that both males on a phyto-oestrogen-rich soy-based diet and those on a phyto-oestrogen-free diet could induce both effects. For subsequent experiments, males were castrated and treated with either oil vehicle or E(2). Enzyme immunoassay was conducted on non-invasively collected urine samples from these males. Concentrations of urinary testosterone were subnormal in both conditions, but urinary E(2) was restored to the normal range for intact males in castrates given E(2). Urinary creatinine was also quantified as a measure of hydration and was significantly reduced in males treated with E(2). Castration diminished the capacity of males to promote growth of the immature uterus and also their capacity to disrupt blastocyst implantation in inseminated females. Injections of E(2) to castrated males restored both capacities. These data converge with other studies indicating that E(2) is the main constituent of male urine responsible for induction of both the Vandenbergh and the Bruce effects.

Oestradiol treatment restores the capacity of castrated males to induce both the Vandenbergh and the Bruce effects in mice (Mus musculus)